Science topic

HIV - Science topic

Human immunodeficiency virus. A non-taxonomic and historical term referring to any of two species, specifically HIV-1 and/or HIV-2. Prior to 1986, this was called human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). From 1986-1990, it was an official species called HIV. Since 1991, HIV was no longer considered an official species name; the two species were designated HIV-1 and HIV-2.
Questions related to HIV
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In the developed countries and transitioning economies, We have seen the rules of lockdown being relaxed so that people are being allowed to go to beaches and other to jog. In some US states, for example people are enjoying their spring out despite the soaring impact of covid-19. Is it time that we accept the virus is with us and learn how to live with it just as the case with HIV? If so what measures must we take to contain spread of coronavirus?
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Countries like Ghana who initially relaxed covid-19 lockdown have seen a surge of the cases and so I agree with Ben Boubakary . However, until when will it be safe to reopen and to what extent will the vulnerable economies of developing nations be affected remains the real concern
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In terms of explaining, will my contextual framework constitute reviews of related literature or sets of graphic charts?
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Nice Contribution Gautam Ray
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I am part of a program that is conducting HIV case identification in a near epidemic control catchment in a resource limited setting. The challenge is that a number of clients are presenting as treatment naive for testing and not disclosing that they are silently transferring to the program to avoid potential hurdles of getting a formal transfer from their current busy facilities.
This behavior is leading to a potential danger of patients being started on inappropriate regimens and treatment failure.
Objectively, rapidly and cost effectively determining which patients who are newly diagnosed as HIV positive have prior exposure to ARVs will provide a means of offering appropriate disclosure counselling and treatment.
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Secondly with changing guidelines based on INSTI based regimens they will be least likely on 3TC
if someboody is on drugs look for nail discolouration, lipodystrophy and osteoporosis due to ZDV, STAVUDINE, TENOFOVIR
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New England Journal of Medicine, 27. February, 2020:
REVIEW ARTICLE
The Modern Epidemic of Syphilis
K.G. Ghanem, S. Ram, and P.A. Rice
📷
Today, the incidence of syphilis in the United States has returned to levels not seen in more than 20 years.
Clinical Pearls Describe the current epidemiology of syphilis in the United States. Since 2000, the increase in rates of primary and secondary syphilis in the United States has been largely attributable to an increase in rates among men by a factor of more than 3; in 2018, men accounted for 86% of all patients with syphilis. More than half of men with incident syphilis reported having sex with men, and 42% of those men were infected with the human immunodeficiency virus (HIV). A second, more recent epidemic in the United States is affecting heterosexual men and women. Rates of primary and secondary syphilis among women more than doubled between 2014 and 2018. The remarkable increase in the number of cases of primary and secondary syphilis among women of childbearing age is mirrored by increasing numbers of congenital syphilis cases and increasing infant mortality. What clinical features of syphilis may manifest at any stage of the disease? Asymptomatic or symptomatic neurologic involvement may occur during any stage of syphilis. Central nervous system (CNS) invasion by treponemes is accompanied by abnormal cerebrospinal fluid (CSF) findings in up to 50% of persons after early infection, even in the absence of clinical features (termed asymptomatic neurosyphilis). Ocular syphilis and otic syphilis are, technically, distinct entities from neurosyphilis but may occur concomitantly. Like neurosyphilis, they can occur during any stage of infection. Morning Report Questions When is routine CSF examination recommended in patients with syphilis? The CDC does not recommend routine CSF examination for persons with early syphilis, irrespective of HIV status, unless neurologic signs are present. A CSF examination is necessary in all patients with neurologic signs or symptoms and in neurologically asymptomatic patients with evidence of tertiary syphilis. A CSF examination is not necessary to diagnose ocular or otic syphilis in patients with reactive serologic tests because up to 30% of patients with ocular syphilis and up to 90% of patients with otic syphilis have a normal CSF examination. Although serologic testing for syphilis in elderly patients undergoing an evaluation for dementia is not routinely recommended in most clinical settings, such testing is frequently performed. Consequently, patients may be found to have reactive serologic tests (a reactive treponemal test accompanied by either a reactive or a nonreactive nontreponemal test). Information about a history of syphilis, treatment, and nontreponemal titers may be valuable but is rarely available. Before CSF testing is performed, clinicians should estimate the probability of syphilis, as opposed to another diagnosis, as a cause of the observed neurologic findings. If the pretest probability is moderate or high, a CSF examination is warranted. What is the drug of choice for syphilis? Penicillin is highly effective for all stages of syphilis and is the drug of choice. Resistance to penicillin has not been observed in Treponema pallidum. Recent shortages of penicillin G benzathine underscore the importance of establishing alternative treatment regimens, particularly in pregnant women. For persons with a documented penicillin allergy, desensitization and treatment with penicillin are recommended. Limited data preclude the use of alternative antibiotics agents, which should be considered only when treatment with penicillin is not possible or is absolutely contraindicated. Ceftriaxone has been shown to have efficacy similar to that of penicillin in all stages of syphilis, although the data are restricted to observational studies. Ceftriaxone penetrates the CNS well and is an option for treating neurosyphilis in nonpregnant adults with penicillin allergy in whom desensitization is not possible.
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Syphilis is caused by a spirochete (a spiral-shaped bacteria) called Treponema pallidum. You can get the bacteria in the following ways:
  • direct contact with a syphilis sore (usually found on the vagina, anus, rectum, in the mouth, or on the lips)
  • during vaginal, anal, or oral sex with an infected person
  • an infected mother can pass syphilis to her unborn child, which can result in serious complications or even death of the unborn child
The primary and secondary stages of syphilis are extremely contagious. Tell your previous sexual partners if you are diagnosed with syphilis so that they can get tested to see if they have the disease.
You can’t catch syphilis from doorknobs, toilet seats, swimming pools, clothing, bathtubs, or silverware.
There is a high correlation between syphilis and HIV, since HIV can be transmitted through syphilitic sores. Since the behaviors that lead to the spread of STIs are the same for both syphilis and HIV, having syphilis is an indicator that you are also at risk for contracting HIV.Syphilis is a sexually transmitted infection (STI). There are four stages of the disease: primary, secondary, latent, and tertiary (also known as neurosyphilis). Primary syphilis is the first stage of the disease. It causes one or more small, painless sores in or around the genitals, anus, or mouth.
If you don’t get treatment for the primary stage of the disease, it may progress to the second stage, which is secondary syphilis. If you aren’t treated for secondary syphilis, the disease will likely progress to the latent stage, and may even progress to the tertiary stage.
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Synthetic sex dolls are presently sold on global scale to replace human commercial sex workers in brothels, where the dolls can be used by multiple users. Can the use of these products increase the prevalence of STDs? Because, the dolls could be used by multiple users, serving as fomite for indirect transmission of STDs from an infected inanimate object to a susceptible person. Are the synthetic sex dolls safe at all?
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It could be possible if the dolls are not strelized after use. Neisseria gonorrhoae is one. Although, nonsexual transmission of gonorrhoea seems to be extremely rare. Only one case of nonsexual transmission of genital Neisseria gonorrhoeae is documented in adults', involving two patients in a military hospital who shared a urinal. N. gonorrhoeae has been shown to survive in infected secretions on towels and handkerchiefs for 20 and 24 hours, respectively.
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The adaptive, or acquired, immune response takes days or even weeks to become established—much longer than the innate response; however, adaptive immunity is more specific to pathogens and has memory. Adaptive immunity is an immunity that occurs after exposure to an antigen either from a pathogen or a vaccination. This part of the immune system is activated when the innate immune response is insufficient to control an infection. In fact, without information from the innate immune system, the adaptive response could not be mobilized. There are two types of adaptive responses: the cell-mediated immune response, which is carried out by T cells, and the humoral immune response, which is controlled by activated B cells and antibodies. Activated T cells and B cells that are specific to molecular structures on the pathogen proliferate and attack the invading pathogen. Their attack can kill pathogens directly or secrete antibodies that enhance the phagocytosis of pathogens and disrupt the infection. Adaptive immunity also involves a memory to provide the host with long-term protection from reinfection with the same type of pathogen; on re-exposure, this memory will facilitate an efficient and quick response.
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Please see the following PDF attachment.
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What is the significance of Pradhan et al from New Delhi’s work?
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The preprint of Pradhan et al. manuscript was withdrawn before publication. Why? No point discussing a non-issue.
bioRxiv shows that this preprint has been withdrawn, it may be due to methodological flaws.
Is this the manuscript you are referring to?
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We will use a survey which contains close-ended questions.
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You may collect data from the respondents using structured questionnaire and test the data using structured equation modelling.
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Dear all, I am trying to retrive from the "Los Alamos HIV sequence database" ONLY the sequence of HIV-1 POL for clade B. Would you be so kind as to tell me if this is possiible ? and if yes how to do it ? Thank you very much, Cecilia
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On the download results page, there is a check box to "clip sequences to selected region" which is checked on by default. As long as you don't check it off, the download will only contain the Pol gene, if you selected the pol gene for your search.
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Hello everyone!
I have been trying to get familiar with R and once I start running syntax everything is fine, but I CONTINUE to have trouble reading data into R. This is an example of syntax I am trying to use. Please, let me know what is wrong with my syntax!
CSDSa = read.csv("C:/Users/jessicabagneris/Desktop/HIV Abuse Paper/HIV Abuse Paper/CSDSa_demographics.csv", header = TRUE)
Error in file(file, "rt") : cannot open the connection
In addition: Warning message:
In file(file, "rt") : cannot open file 'C:/Users/jessicabagneris/Desktop/HIV Abuse Paper/HIV Abuse Paper/CSDSa_demographics.csv': No such file or directory
The file exits and I am in the current directory per my Getwd command output that I copy and pasted.
getwd()
[1] "/Users/jessicabagneris/Desktop/HIV Abuse Paper/HIV Abuse Paper"
Honestly, this happens every time I start working with new data...
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At first, make sure that R can see the file
file.exists('your file path')
Option1: Using backslashes
read.csv('C:\\Users\\jessicabagneris\\Desktop\\HIV Abuse Paper\\HIV Abuse Paper\\CSDSa_demographics.csv', header = TRUE)
Option 2: Using manual file selection
read.csv(file.choose())
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Have heard a handful of anecdotes from Spain (and also now here in NYC) that HIV-infected persons on antiretroviral therapy appear to be less likely to contract Covid-19.
And, of course, as a corollary to this, I am wondering if HIV- persons taking emtricitabine-tenofovir ("PrEP") might also be.
Thirdly, there is the question of, contrary to popular presumption, HIV-infected persons due to unresolved aberrations in cell signaling or other unresolved immune defects might not advance to the most lethal extremes of infection, were they to become infected.
Best resource of data at this point, one might imagine, would be from countries in East Asia that appear to be coming out of (at least the first wave of) this. There are great community based HIV networks I am aware of in Spain, Italy, Germany, UK, others, but I hesitate to ask this of them now. But it seems important for many reasons. Tk u, Mike
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The more "evolved" statement of current theory: that key protein/proteins on surface of Sars-Cov virus resemble/s similar protein/s on surface of hiv to an extent that the immune response of an hiv-infected person (with relatively in tact immune system) already kind of recognizes this new virus. Probably not 100% protection, but more like a vaccine that provides, what is it? 70 or 80 or even 90% protection?
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It would be very helpful if someone can send me a link or text containing the list RNA dependent RNA POLYMERASE (RdRp) inhibitors.
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What is the temperature required for storage of samples (serum) before HIV, HTLV 1, HBSAg and HCV tests with ECL technique?
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In a good freezer maintained at minus 80 degrees Celsius
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I need to distinguish HIV integrated DNA, from HIV unintegrated and HIV-mRNA. For the first 2 ALU-LTR PCR works well and shouldn't be a problem because mRNA can't be detected without RT reaction, so basically doing 2 independent reactions the problem is solved.
The problem is that for my experiment flowchart, I can't take the sample before cDNA reaction (RT) is done... so I had already the mRNA transformed into cDNA...
My only doubt is if HIV-mRNA had ALU elements within or not, if not, there's no problem to use ALU, but in case the ALU elements are present in HIV-mRNA, I will not be able to distinguish from mRNA and integrated DNA.
Greetings
Gibran Horemheb
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Hello, this article could be useful for you:
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HIV patients are at high risk due to a weakened immune system.
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Sorry, but the correct name is Cystoisospora belli.
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If I were to plan an experiment to deduce whether or not PD-1 is absolutely necessary for HIV to establish latent infection in CD4 memory cells, how would I go about doing this?
More specifically:
  1. Would the approach of incubating HIV particles with either a) WT CD4 memory cells or b) PD-1 negative CD4 memory cells be sufficient? I understand that I would have to define which subset I was focusing on, given the heterogeneity of these cells.
  2. What is the appropriate source of memory cells? i.e, extracting memory cells from a human and then deleting PD-1 vs. using some sort of CD4 memory cell line.
  3. Is proviral integration a sufficient marker of latency?
Many thanks!
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HIV tropism
It's refers to the type of cell that the human immunodeficiency virus (HIV) infects and replicates in. HIV infects human immune system cells such as T cells (specifically CD4+ T helper cells), macrophages, and dendritic cells.
Entry of HIV-1 to macrophages and T helper cells, is mediated not only through interaction of the virion envelope glycoproteins with the CD4 molecule on the target cells but also with its co-receptors.
Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use CCR5 receptor for entry and are thus able to replicate in macrophages and CD4+ T-cells. These strains are now called R5 viruses.
T-tropic strains, or syncitia-inducing (SI) strains replicate CD4+ T-cells as well as in macrophages and use the CXCR4 receptor for entry. These strains are now called X4 viruses.
Dual-tropic HIV-1 strains: A strain of HIV that can enter and infect a host CD4 cell by attach to a CD4 receptor, then attach to either the CCR5 or CXCR4 coreceptor on the CD4 T lymphocyte and finally fuse its membrane with the CD4 cell membrane. HIV is usually R5-tropic (uses CCR5) during the early stages of infection, but the virus may later switch to using either only CXCR4 (X4-tropic) or both CCR5 and CXCR4 (dual-tropic).
Viruses that use only the CCR5 receptor are termed R5, those that only use CXCR4 are termed X4, and those that use both, X4R5.
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Being that the MARS was originally developed to measure medication adhere among psychiatric patients, would it be appropriate to use among another group of patients, like HIV Patients?
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Than you Peter Bai James
I think the second option will be most appropriate for me because of time constraints. Appreciated
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We are comparing the incidence rate of two age groups in a cohort study; those under and over 50 years of age. As patients age, they will pass from one group to the next, so their count for some person-years in the first group, and than the second. Is there a way to adjust for the time since they are in the cohort?
In this particular case, we are dealing with HIV patients, so as patients become infected, they will be included in the cohort, and during their follow-up they might have some sort of event due to the infection. What I'm wondering is, if a patient has an event at 52, and counts as 0.5 person-years for the >50, is there a way to adjust for time depending on when this person was infected at 58 or at 30 (so, in essence, to adjust for time since infection)?
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if you take this approach, alternative methods would be to restict study to comparable exposure durations or to use regression modelling with length of exposure as a covariate.
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The human immunodeficiency virus (HIV) can be transmitted via unsterilized objects, blood transfusion, and some other blood/fluid related substances. From the mosquito perspective, the vector sucks blood and may instantly suck that of another. Supposing it sucks a HIV carrier and immediately sucks another person (A non HIV carrier). Will the HIV be transmitted or what would happen to the non-carrier? Or is there a substance that would hinder the transmission of the VIRUS?
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Please, a general remark to all RG member who are not so familiar with biomedical issues: PubMed (https://www.ncbi.nlm.nih.gov/pubmed) is the best soruce of information. But please be careful: You need to cross-check the reliability of the information provided! Don´t believe all information!
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Hello, I'm a graduate student working in a lab as part of my degree.
I am currently trying to calculate TCID 50 values using HIV pseudovirus and TZM-bl cells. To my understanding, I need to score wells as positive or negative using a luciferase activity cutoff, however I don't understand how a cutoff is chosen. I found a few articles using a cutoff 2.5 times or 3 times the signal of the cell control wells. Can I simply use a similar multiple, or is there a way to calculate the best cutoff each time?
I have attached the articles in question with relevant sections highlighted.
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As the luciferase activity is very variable per se, you may get a big SD. So it is recommended to repeat the assay more than three times to get a cluster for the luciferase activity. Having more number of experiments help to identify the outliers in your assay. Then you can use MEAN ± 2SD tp set your threshold.
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I am really interested in the question of the rights of HIV positive persons.
Can you help me to find some acts of the higher courts about the problem of applying the rules of adoption of children by the person HIV positive?
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I'm doctored in law, but this is not my speciality. I think you can consult cases-law and judgment and decisions on this matter in the European Court of Human Rights (for example).
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In my work on ARV adherence in Botswana I have often noticed that PLWHA receiving their ARVs in plastic bottles are annoyed of the shaking noise the tabletts make inside of the bottles. Especially when using public transport this poses a problem of beeing recognized as HIV+. Has there been research done on that topic? Does somebody have simliar experiences in their work?
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I have had it expressed as a deterrent and wondered if you have other research reports stating the same
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I have used about 9 markers to examine NK cells by flowcytometry in HIV Vs Healthy controls. Can I get how a justification on which small sample size is enough for such experiments?? Or what is the least minimum participant I have to use????
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Hi Henok,
Completely agree with Fatma Abdel Wahab and Dmitry Zinovkin . You have to do power calculations to determine your sample size. If you are measuring the expression level of markers expressed in NK cells, you need to have some estimation or idea as what difference you expect between your control and patients' samples. In some cases it might be possible that you will need less that 15 samples,. Or maybe you will need more is the expected difference is very small. Try this online tool:
Regards
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I am currently doing my thesis entitled "Career Perspectives of Persons with HIV" I really need a survey/questionnaire regarding this topic.
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It might be useful to consult existing Stigma scales (e.g.:) and extract the items related to employment
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I currently use calcium phosphate to transfect multiple plasmids into HEK293 cells in order to generated the chimeric HIV virions I use, but calcium phosphate does not work well a large percentage of the time. I was wondering if anyone knew of a better/more efficient/more consistent transfection method for virus production from HEK293 cells, especially using multiple plasmids to generate the virus. 
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High active antiretroviral therapy (HAART) can save life of a lot of HIV/AIDS patients. It is the standard of care for HIV infection.
However, HAART has serious side effects and drug-resistance for HIV. It needs HAART intervention adherence, life-long and there is no cure.
In order to better serve HIV infected patients, we argue which is more effective? Early treatment (as soon as HIV diagnostics) or later treatment (patient CD4 is greatly declining)?
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An excellent explanation of the rationale for early and continuous treatment is given at http://hivmanagement.ashm.org.au/index.php/therapeutics-and-monitoring/antiretroviral-therapy (from paragraph 3). Essentially, this is associated with better clinical outcomes across various measures, as well as prevention of sexual transmission if viral suppression is achieved. Prevention of transmission ("undetectable = untransmittable", see https://www.unaids.org/en/resources/presscentre/featurestories/2018/july/undetectable-untransmittable) assists the public health response and efforts to end the HIV epidemic (for example, UNAIDS targets). Apparently the most recent therapies have fewer side effects, and taking them consistently as prescribed reduces the risk of drug resistance (https://aidsinfo.nih.gov/understanding-hiv-aids/fact-sheets/21/56/drug-resistance).
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Hello everyone, I am working on a project for hiv 1 integrase. I have performed cloning and according my seq results it was successful. It has been few weeks I’m trying to detect my protein on western but it doesn’t show up. Hiv 1 integrase is getting degraded so I am using proteasome inhibitor(mg132). I have tried several treatments but none of them has worked. I did 50ul for 3 and 4 hours, 20ul for 4 hours, 10ul for 8hours and 6hours, 2ul for 18hours. I seed the cells and thennafter 24 hours I make the transfection with my pcmv5 flag integrase plasmid and then after 24 hours I start the treatments. Cell line used is Hek cellsZ any advice is valuable. Thank you
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First you can try with the dotblot .......if it works then go for westrenblot................................
I think the epitope is not available to bind by mAb
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I am going to meassure STDs by ELISA (HIV, herpes, hep a and b and syphillis) but from the point of sample collection to the lab there is a long distance. How can I overcome that? Do I hve to keep the whole blood samples at a certain temperature so the results are valid? What can I do?
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Hepatitis A is not a STD.
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Does anybody know if there are antibodies targetting HIV TAT-peptide (just the region used for transduction: GRKKRRQRRRPQ)
We wanted know if our TAT-peptide has entered the cell by Western Blott but we are not sure if it is possible.
Thanks in advanced!
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You should check the NIH AIDS Reagent Program (https://www.aidsreagent.org/search_reagents.cfm). In addition to Creative Diagnostics mentioned by Jiang, there are a number of other commercial sources for anti-HIV tat, though specificity for just the transduction region you want may be hard to find: Antibodies-Online, Invitrogen (ThermoFisher), Novus Biologicals, BioLegend, LifeSpan Biosciences, St John's Lab, US Biological etc.
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A single mother and a female sex worker have the same risk of been infected with HIV and others STIs?
This is the main result of a research conducted in Zambia
"Single Mothers and Female Sex Workers in Zambia Have Similar Risk Profiles".
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Just read the abstract - the results are convincing, although statistics are not given in the abstract.
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I am planning to start a molcuar diagnosis lab. I would like to buy a real time PCR platform for viral detection and quantification
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Dr Chandran,
If your funds permit, consider going for a droplet digital PCR. It has lot of advantages over conventional Real Time PCR.
regards,
SD
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Alarming surge in drug-resistant HIV uncovered. Honduras is one of the first according to survey. The drug-resistant form of the virus has been detected at unacceptable levels across Africa, Asia and the Americas. But if the application of these medicines has been going on for years, why is this known so far? Is there no follow-up of cases in each country?
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Dear many countries may not monitor the response because microorganisms are known with mutations and other strategies to thwart the effectiveness of chemotherapy.
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Nice one @Segun Michael Abegunde for that question...
My own Question is are there people who are naturally immune to HIV?
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Yes. Please see the below given RG link and PDF attachments.
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Hello,
I am working with limiting dilution PCR amplification of a 3 kb HIV gene and I would like to ask how the extension time could affect the number of my bands. More specifically, when I shortened the extension time from 4 to 2 minutes, I realised that I was getting fewer bands of the right size than with the longer extension time. Could someone give me an idea of why could that be happening?
Thanks!
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if more of your samples are amplifying at the longer time then I think that you are using a standard polymerase which is liable to extend then fall off before the extension is complete and the DS/SS dna strand then has to wait for another taq molecule to bind to the ds/ss junction and continue to extend the amplimer from the internal fail point to the end of the amplimer. This slows down the theoretical extension time ( often about 100 bases/second for normal Taq). The yield would then be increased either by increasing the extension time to allow re annealing or by using more polymerase so that it binds the strand quicker. More taq usually means more non specific bands so an increase in extension time even to 5 minutes may improve the efficiency and give better results
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Hello everyone,
I would like to some experiments with different HIV bNAbs but I can not find any supplier .. I mean except the NIH Reagent programme, does anyone know where we can purchase HIV bNABs ...?
Thanks in advance for your help !!
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Does anyone try to using PSPAX2 and PMD2G to packaing the lentivirus of HIV1 -EGFP(backbone)?
I search the standard protocol of lentivirus of HIV1 -EGFP, they use VSVG, pMDLg/pRRE and pRSV-Rev three helper plasmid.
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I‘ve used pEZ-Lv201, a HIV1 based 3rd vector, with PSPAX2 and PMD2G for packaging lentivirus. This system worked well, both in 4:3:1, 4:2:1 and 9:8:1.
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I am searching for articles that talk about the denialism of HIV in South Africa
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I have been seeing HIV positive female  patients  in whom it seems developed ammenorhea /oligomenorrhea when they were commenced on Anti retroviral therapy. Or it is the effect of the HIV virus itself?
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Please take a look at this useful PDF attachment.
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How to overcome the unequal sample size problem in convergent parallel design? e.g. using snowballing technique quantitative samples reached 160, and only 25 of 160 samples agreed to participate in qualitative interviews. (subject is HIV patients)
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I've never liked the terminology "convergent parallel" designs because things that are parallel never converge. To me, convergence by itself summarizes the goal in such designs, but so be it.
With convergence, the key goal is to show the equivalence of the results from a qualitative and a quantitative study of the same research question. Each method should be 'self-sufficient' in the sense of meeting the appropriate standards for that type of method. Hence, there is no need to generate an overly large sample for the qualitative portion of your study.
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Hi all,
I was wondering if anybody has any advice on how to stimulate PBMCs isolated from HIV+ individuals so that I can extract DNA for amplification, please.
Many thanks,
Peny
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That’s interesting! Are you going to traditional Sanger sequencing or next-gen high throughput sequencing methods?
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The key points of the focus groups were as follows: Experiences/issues with the HIV diagnosis, treatment and medication; Challenges of living with HIV, e.g., health services and community life; Stigma and segregation of people living with HIV.
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I think the current burden depends really on the contexts. It is obvious that the challenges living with HIV in rural sub-Saharan Africa will be different from living in London with the disease. So health systems, healthcare delivery, social determinants, persisting issues of stigma and social exclusion, employment related issues, access to medicine, regular monitoring of CD4 count etc. This will really depend on the location of the individual.
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I am looking for good resources of phisiological plasma concentrations of diverse cytokines in humans. I want to compare them with those of a cohort of HIV+ patients (very late presenters).
The cytokines I'm studying are:
IL12p70, TNFalfa, IL10, IL6, IL1beta, IL8, IL-18
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Dear collect blood samples from apparently healthy individuals from your area of study and establish your reference range because it is relative based on area of study from there you compare with your case samples.
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Dear scientists,
Health workers in my country preach that preventive measures of HIV/AIDS such as use of condoms, abstaining, testing and circumicision. Is circumicision scientific tested as a preventive measure of HIV?
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Most studies on the subject have shown tht circumcision reduces transmission to the male partner by up to 60%. However, there is no evidence tht it reduces transmission from males to females.
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kindly help me for the cryopresevation for FNA from HIV+ve pt Lymphnode.
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my FNA sample will be 0.5ml if i dilute with PBS in 1:2 ratio and over lay in equal amout of Ficoll or Histopaque will it give the result..
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For example, for HIV drugs, there are many studies going on. Let's just say one is targeting glycoprotein A and another one is targeting another protein. Are these two drugs considered as competing with each other? Or as long as they are treating the same disease they would be competitor? Thanks!
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For your example, Yes because the outcome is the treatment of the disease. But in a case where one will complement the other, there it can’t be a competitor.
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We can control bacteria and fungus easily whereas it is very difficult to control virus. Even, there is no control of some viral diseases and virus, e.g., HIV. Why is it difficult to control viruses?
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Bacteria can be killed because they are independent cells living outside of our our cells. Antibiotics can be found that are toxic to them but not to our own cells.
Viruses are obligatory parasites. They use the mechanisms of our own cells to reproduce, so if we find a chemical that stops the virus it generally also stops our own cells. Viruses function inside our own cells so any chemical that attacks them has to get inside our own cells.
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Does anyone know about miRNA that prevent of the viral genes specifically with the least disruption in other important genes?
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Hi Masih Nazari , that's like asking if anybody knows of a new antibiotic that can kill resistant bacteria without side-effects. If there was anything like that, we would all have heard about it by now, don't you think?
If you are interested in the subject, a Pubmed search would probably be a better starting point. You can try searching for "HIV AND miRNA" and see how much has been done already.
This review is also a good primer.
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After over a decade of seeding small(er) scale 293T fresh from ATCC I can say with confidence that Invitrogen (HeLa based) chart never really worked out for me to obtain 70-80% for 293T, the significantly smaller cell body size affects the seeding a lot.
I've now developed counting-based seeding for most small scales that are highly efficient but I would be curious to know if people have experience (from counting) of densities that work for real large scale volumes and compare. I'm currently playing with a lot of formats and among them are multi-layer flasks like the Nunc triple layer flasks (500 cm2 area). Talked with people who work with the Corning 10 layer stacks which you can't check under the microscope anymore - and their numbers seem extremely high for seeding.
So for those of you who do counting based in large volumes & areas (lets say at least 150 mm plates): could you give a number of how many cells you seed in what volume of media for 70-80% confluency 18-24h later? What about 70-80% 42-48 hours later? Are your 293T fresh from ATCC or are they long term circulating in your lab (cryo, freezing, thawing again, starting batch number at 1 again maybe)?
Thanks!
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Dear Ulrike,
Typically, for lentiviral production, the recommend cell density of 293T/T17 (ATCC) is 80% confluency, which means roughly 240,000-280,000 cells/cm2. To get this confluency, 140,000cells/cm2 should be seeded in DMEM with 10% FBS at 24h in advance, while 70,000cells/cm2 at 48h ahead.
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Among HIV positive patients, is it possible that non-AIDS diseases alter the risk of developing AIDS and vice versa?
For a HIV positive patient who has experienced a non-AIDS disease, Does the treatment for non-AIDS diseases reduce the risk of developing AIDS?
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Dear Sahar Nouri,
Non-AIDS diseases alter the risk of developing AIDS and vice versa.
The treatment for non-AIDS diseases reduce the risk of developing AIDS, if the treatment takes into account avoiding unnecessary turnover of CD4+ T cells as mentioned in Dr’s Tetsuo Tsukamoto answer.
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Just need to know physiology of a cell of these races
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Dear Africans are at greater risk because they have the CCR5 unlike the Europeans who are deficient of the factor giving them selective protective advantage over HIV infection.
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Is mandatory HIV testing in Health Institutions the quickest way to reduce HIV transmissions in Sub Sahara Africa ? What would the the effect on pre test HIV counselling.
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Support for hospital-based HIV testing and counseling:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1382157/by JA Boscarino - ‎1995 - ‎Cited by 4 - ‎Related articles These include hospital support for voluntary HIV testing and AIDS education and the impact that treating AIDS patients.
I think Early diagnosis will reduce the spread of HIV because the patient will seek treatment and avoid more infections.
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I am currently creating a direct ELISA to measure an HIV protein in a viral vector. I'm using the formulated buffer to generate my standard curve, and it works beautifully. However, when I do spike recovery experiments in the vector itself, I only recover approximately 10-20% of my input. I did a dilution series of vector to buffer down to 1:2000, and I continue to get the same OD values no matter the dilution. Does anyone have experience with this? I've never done an ELISA with a viral vector, so this step is new to me. I know the vector is interfering, but based on my results, I don't know how. Any advice at all would be greatly appreciated!
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MAY BE DEPENDING OF TYPE KITE THAT USED
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I was asked in an interview by a doctor.
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AIDS cannot be transmitted. AIDS is a diagnosis, a syndrome, a collection of disease. HIV is what is transmitted and as Kannan has mentioned it depends on the viral loads of the women living with HIV. According to the CDC, people diagnosed with HIV who are in care and treatment and who achieve and maintain an undetectable viral load have no risk of transmitting HIV to their sexual partners.
HIV transmission also dependents on the types of sexual behaviors the persons engaged in, if condoms were used correctly, if the male was circumcised, and if the partner had another STI. Anal sex increases the risk of transmission to the "bottom" (male or female partner) if the "top" partner is diagnosed with HIV. With that said, biologically speaking, it is more challenging for a women to transmit the virus to a sexual partner than it is for men to transmit HIV. HIV needs to get into the blood system in order to "infect" the cells of the partner who is negative. If condoms where used correctly during the sexual acts, then there is also a lower risk of transmitting. Cameron, (1989) indicate an extremely high rate of female to male transmission of HIV in the presence of another STI. According to Beaten and colleagues (2005) uncircumcised men are at a <2-fold increased risk of acquiring HIV-1 per sex act, compared with circumcised men.
Boily, et al., 2009 found that, overall, female-to-male (.04% per act or, in theory, about 4 cases of HIV transmission per every 10,000 acts of vaginal sex with a woman who is diagnosed with HIV). Beaten and colleagues (2005) looked at other studies and found that "the probability of female to- male HIV-1 transmission for a single act of penile vaginal intercourse was estimated to be on the order of 0.001 or less. A small number of studies have estimated female-to-male HIV-1 transmission risk in more transient partnerships—specifically, prostitute contacts—and these studies generated infectivity estimates <30-fold higher (0.03–0.08)."
Baeten, J. M., Richardson, B. A., Lavreys, L., Rakwar, J. P., Mandaliya, K., Bwayo, J. J., & Kreiss, J. K. (2005). Female-to-male infectivity of HIV-1 among circumcised and uncircumcised Kenyan men. The journal of infectious diseases, 191(4), 546-553.
Boily, M. C., Baggaley, R. F., Wang, L., Masse, B., White, R. G., Hayes, R. J., & Alary, M. (2009). Heterosexual risk of HIV-1 infection per sexual act: systematic review and meta-analysis of observational studies. The Lancet infectious diseases, 9(2), 118-129.
Cameron, D. W., D'Costa, L., Maitha, G., Cheang, M., Piot, P., Simonsen, J. N., ... & Plummer, F. (1989). Female to male transmission of human immunodeficiency virus type 1: risk factors for seroconversion in men. The Lancet, 334(8660), 403-407.
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Mosquito bites are similar to injection directly in human body
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I want as part of my job, research the faceturs associated with HIV in 2015 and 2017 and compare the odds ratio over these two periods. My concern is that the sample is not the same. I would like to know if there is an opportunity to do it.
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Remember to take into consideration the 95% confidence intervals of the ORs you wanna compare.
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I am working on a systematic review for my masters thesis. The systematic review will evaluate and assess vaginal microbicides research from a gender perspective.
I am currently looking at SGBA tools and checklists for the evaluation of gender integration/ sensitivity throughout the research process; however, the tools I am finding are more appropriate for research conducted on both men and women.
So please if anyone has any ideas/ tool/ checklists that are suitable for this project let me know. Thanks!
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Ghose Bishwajit Thank you for your answer. The aim of the study is to evaluate whether or not the research process has taken into account all gender related variables that may hinder the real world application of VMs in sub-Saharan Africa. For instance, women have less power in relationships, low autonomy (in terms of freedom of movement, decision making, and allocation of funds), etc. In many VM trials and studies, the analysis did not stratify the sample by SES, age, gender dynamics between the women and her partner. Also, many acceptability studies have excluded men from the sample even though it was proven that women's ale partners play a major role in their adherence to the VM.
I hope this has clarified it a bit. Kindly let me know if you any ideas. Thanks!
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It has been written many times by different scholars that it was unlikely for infectious viruses such as HIV and Hepatitis B may not be able to transmit these viruses from one person to the other.
How possible can we prove that this theory may not be accurate?
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Dear a recent research should be conducted in this case and it may surprise you that the pattern must have changed.
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A step in developing vaccine for HIV virus.
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آسف السؤال ليس من اختصاصي
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Good day, I have been able to prepare stocks containing HIV-1 pure, frozen in liquid nitrogen in cryovial tubes. For the purpose of my research, I need to quantify the virus to know how much particles/mL I have present to infect my cells using a multiplicity of infection of 1.6.
How can I do this? Do I need to treat my virus with Trizol to extract the RNA and then use a primer that is specific for, let's say, coding of p24 and perform RT-PCR?
How could I treat my virus? I have it in 1mL stock in cryovial tubes.
Thank you.
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Jack Greenhouse thank you very much.
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Anti-Retroviral Therapies (ARVs) administered in the HIV positive individuals suppress the viremia as soon as 3 months after start of ARVs. HIV molecular characterization on the basis of its genome is very important to analyze the mutations and CRFs in the population. I am working on HIV population from Pakistan and all the adherent individuals have suppressed viral load. In such case, how can we extract HIV RNA dn Pro-viral DNA for downstream applications of NGS?
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Take more input amount of cells/plasma to isolate RNA, DNA and use recommended kits for isolation.
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Data of the diseased Patient can be collected from WHO and their test cases so that information can be given to Artificial Intelligence. AI will use Combination and Permutation as the result life span of patients can be improved.
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Ragavanantham C. : Are we talking about artificial neural network(ANN) here?
ANN has been widely used in various fields even in India.
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I'm conducting a cross-sectional study of emotional development in adolescents impacted by stigmatization following an HIV diagnoses. I need an effective instrument, or empirical methodologies open for redesign, to undergo the study.
So far I have uncovered a few that can be of help, but would appreciate an experienced individual sharing their insight.
Thank you
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It seems that you need to develop your own scale to measure what you really want to assess, through multidisciplinary nature of literature review. Psychological variables as well as other behavioural variables should be included. Need to do qualitative research as well.
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Please, can someone provide me with this book:
"Numerical Methods to Solve Fractional Order Optimal Control Problems: Numerical Simulation of Fractional HIV Models Using Some Numerical Methods"
Thank you
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Thank you Dr. A. M. Abdallah.
If you can obtain the book please send to me.
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I have a set of HIV pol sequence data, and after alignment it is clear that some sequences are much shorter than others – primarily due to sequencing issues. Because the gaps/missing data are not necessarily meaningful, I consider these a "complete deletion" when doing a maximum likelihood phylogenetic analysis. Doing this, however, reduces the number of positions that could be included in the analysis since only positions where there is data for all sequences can be used. I was wondering what the best approach to handle this would be. Is there a general lower limit for the number of bases that should be included for an informative viral phylogenetic analysis, and is it better to remove samples with shorter sequence lengths? Would a Bayesian approach using programs like BEAST overcome this? Thank you!
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There is no set answer to this type of question. It depends on what type of organism you are studying, and even which gene within a given type of organism. It also depends on what information you want from the phylogeny. For HIV-1 M group viruses, for example, the pol gene has less phylogenetic signal per 100 bases than the env gene does because pol is under much more purifying selection pressure to retain functions (protease, RT, integrase, RNAse etc) and less selection pressure from the host immune system.
If you only need to know what subtype the virus is, a few hundred bases of the pol gene can be enough, but if you want to infer transmission networks you will need more data. Recombination and other issues also create problems. Many HIV researchers now create database entries of two regions of pol (protease and the core of RT) spliced together without noting that there is missing data between the two regions.
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Hi everyone,
I have been searching and searching for the latest HIV global figures for the 15-24 years old age-group. Esp. new HIV infections & prevalence. As I am doing a research project with this group. I have searched the UNAIDS Info site; UNICEF site - including use of these search terms "UNICEF analysis of UNAIDS 2017 estimates" - as I believe these are the latest figures by UAIDS in July 2018. No luck.
I am only able to find regional, sub-national, and national figures. Plus, most of the global data for the 15-24 years age-group appears to be aggregated for mainly young women. Whereas I need latest global data for the entire group.
Avert (see link below), seems to have a useful pie-chart - above the heading 'Why are young people vulnerable to HIV?' But whether these are global or regional figures, and the exact source of data is unclear. The chart only cites UNAIDS 2017. And the reference list in document has several UNAIDS 2017 works - which I have searched to no avail.
Any ideas of where to look would be appreciated.
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Dear Carol,
Your best source of that information is still the UNAIDS website.
Use this link to access all you need:
Just patiently navigate the links there.
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Good day, I need to perform a viral load analysis to quantify the number of viral particles/mL found in my samples. The virus that I will be working is with the Human immunodeficiency virus type I. I was wondering, how do you perform a viral load analysis? I have my samples per mL frozen in liquid nitrogen, where do I go from there for quantification?
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Dear Alvarez, please can you clarify what information you are looking for. When you said samples, is it a plasmas samples or lymphocytes celles samples. If it is a plasma samples, I don't know if it is a god idea to keep them in the liquid nitrogen for futur viral load testing (Copies/ml). Also when you said viral load analysis, do you want to performed viral load test. If yes, you can find many commercials kits in the web, you will just need to follow the manufacturer recommandations, or if you prefer in house made test, that will be another challenge. As you said particles/mL, perhaps you want to determine the HIV-1 title of your samples?
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Isoniazid preventive therapy has been recommended for all HIV patients with latent TB in Nigeria, but there is no little or no monitoring of adverse drug reactions. Therefore the need to monitor the adverse effect of this drug which is used concomitantly with other drugs in people living with HIV and to ensure that it is safe for use.
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OK, thank you@ Emmanuel Ifeanyi Obeagu
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The responsibility of the schools
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The child process and family condition should be kept confidential.
The children should be treated and integrated normally ,because
 the virus, as it is known is not transmitted, by social contacts. Then there are three questions: 1) Non-carriers of the virus and coming from a functional family; Only need the same affection of all the others 2) Carriers of the virus and coming from a functional family , talk with parents and counsel with family doctor 3) Carriers of the virus and coming from a non-functional family: Advise with family doctor and school psychologist.
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Our team had been trying the procedure that is outlined in "Direct PCR: a new pharmaceutical approach for the inexpensive testing of HLA-B* 57:01" study to detect HLA-B gene on HIV patient samples with a in house method, but i have a question.
Whenever we did the gel electrophoresis for the First step PCR and Second step PCR samples, we did not observe any LOXL gene at 444 bp for our negative samples.
A few times we got lucky and we were able to see the LOXL indicator gene, but when we looked at the nested PCR gel electrophoresis result for the same sample, we couldn't see any LOXL internal control genes.. Do you by any chance know the reason why we can't get a consistent result for our negative samples?
We have checked our temperatures, material qualities including our primers etc. Thank you.
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Dear Rukiye,
It is always a little bit difficult to make PCRs with four or more primers.
(It could take a long time to establish a new multiplex PCR system!)
In every PCR system you could need a little bit different primer concentrations.
I would guess, that you take primer concentrations from this publication.
In this case you should vary your primer concentrations in your system.
Perhaps you would need higher concentrations for the primers of your control amplfikat?
Best reagrds,
Thomas
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Men are glaringly absent from the ranks of those who know their HIV status and then act to get care. Is your project investigating that question among the refugees you are studying? Men 39-50; male youth 15-24?
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Hi Eric, thanks for taking the time to respond. The literature from all over Subsaharan Africa including Uganda tells the same story. Getting out of the clinic seems to be advised....Was hoping to get insight on new ideas. Let me know when you hear of/try new things!
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I was looking conduct a cross cultural study on co-morbid neuropsychological conditions in patients with HIV/AID for my PhD. Hence for I was looking some on going study and researchers with whom I can collaborate my research and latter on draw a compression of both the data.
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Thanks for showing your interest in this project and for sending articles, these articles are really helpful.
Regards !!
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Can the genome of cells that harbor HIV be altered to prevent future infection resulting in complete depletion of HIV reservoirs using CRISPER technology with conventional therapies? Can this be done safely? Your thoughts on this.
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It has been successfully used! The other method I am aware of is use of HDAC inhibitors such as valproic acid.
Link to article here:
Open access article:
Ophinni Y, Inoue M, Kotaki T, Kameoka M. CRISPR/Cas9 system targeting regulatory genes of HIV-1 inhibits viral replication in infected T-cell cultures. Scientific Reports. 2018;8(1):7784.
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We know which are targets for HIV virus but not much is known about their passage to them. Is there any research or discussions ongoing on that topic?
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Very interested in this. Whether through inter-cellular spaces, directly onto dendrites of DCs or transcytosis; cell free or cell bound.
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I am trying to analyze an optimal control problem where the control system is a mathematical model for HIV transmission. The objective function involved in minimizing of the number of HIV infected (unaware infected and aware infected) as well as the cost for applying control strategies (education, screening and therapy).
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Get the book titled Optimal Control Applied to Biological Models by Suzanne Lenhart and John T. Workman. This book contains several m.file codes using FSBM ( Forward Backward Sweep Method). I also encourage you to visit her web page for more m. file codes.
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I need an HIV replicons which lack genes necessary for virion release and spreading infection in cell culture but which can replicate intracellularly and may produce some of the HIV proteins.
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As above - good luck as interested in answers.
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I am trying to amplify nearly 9.2kb fragment of HIV genome. The samples are whole blood spots that are dried. Extraction of genomic DNA and RNA (total nucleic acids) is done using the Nuclisens easy meg. The cDNA was prepared using Superscript IV (Thermo) followed by Nested PCR. No amplification. I do not know how to check if the cDNA is of 9.2 kb size. Can anyone guide me to optimize the amplification of 9.2kb fragment?
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Thanks Dr. Foley for your valuable suggestions. We may think about SGA.
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stigma measuring tools
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You could modify one used for studying stigma in cancer patients found in
Asia Pac J Oncol Nurs. 2017 Apr-Jun; 4(2): 155–161.doi:  10.4103/apjon.apjon_10_17PMCID: PMC5412154PMID: 28503649
Reliability and Validity Study of a Tool to Measure Cancer Stigma: Patient Version
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It is well known that low "current" CD4 count is correlated with decreased life expectancy among HIV infected people not on ART. It is also well known that CD4 counts vary hugely within the population of HIV negative people. The question is: is the life expectancy (~ natural disease progression) upon acquiring HIV infection the same for someone who had 1200 or 600 CD4 cells prior to infection?
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A disease that means it was caused by once genetic default by either onco- protein or viral- onco protein. .At first, the DNA/RNA confirmation is very important. The treatment arm should be consider on last symptom.
The last symptom that means a RNA virus /its viral protein or RNA cell-proteins in our cells are randomly (location based) virulent and would be affected to the DNA stranded "proteins". So, subsequently the last symptom will pave way the confirmation either RNA or DNA symptoms.
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Dear Researchers,
I'm designing an interdisciplinary study (with Public heath, Statistics, Psychology etc) on diseases, stigma, discrimination, mental health and quality of life.
So I'm a bit confused that what should be the ultimate construct for human life, I mean what must be there for a human being?
Quality of life is sometimes observed secondary, primarily they should have a moving life.
The whole United Nations (Sustainable Development) Goals talking about Society and people's wellbeing.
But whats the 1 most important factor for humans?
Please provide your thoughts?
Best Regards,
Abhay
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First, I would keep a distance from sustainability concepts, concerning human life quality (because this burns down to economic reform in a capitalist system=systems maintenance). Second, the human bias is built into every questionnaire, concerning life quality; it is always built on the subjective perspective of the interviewer. Third, I do think, all research that is based around happiness is a good starting point for your work; most foundations do apply a happiness index, and this indexes could be methodically compared.
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I am looking for survival curves for infants infected with HIV, differentiated by those who are born with HIV and those who acquire HIV through breastfeeding. In particular, any curves that go out until 0% still alive.
Many thanks
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Dear Tessa,
thank you for asking this good question. What we need to know is that even normal children immunity can be easily suppressed. visit this link for your answer:
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Is it because Rev protein has some special traits that making it difficult to study?
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Hi
One thing i can tell yes the protein itself is a bit crazy. It oligomerize quite often, over expression leads to cell toxicity. As absence of Rev stops HIV replication completely , its highly conserved, i too wonder why researcher are not looking this as a candidate. Some earlier reports are there for Rev inhibitors but they may also influence normal cells also, so no further progress.
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I have a plenty of qualitative data analyzed on deedose I would like to link with quantitative data collected through questionnars and not entered on deedose ( on the same project on migration and HIV)
Do you have any practical recommandations ? Thank you
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From the home page for Dedoose,
Dedoose is a cross-platform application for analyzing qualitative and mixed methods research with text, photos, audio, videos, spreadsheet data, and it supports the following files format
  1. Text document formats include: .doc, .docx, .rtf, .txt , and .pdf.
  2. Spreadsheet formats include: .xls, .xlsx, and .csv. These can all be directly imported to the Descriptor Workspace and code tree depending on your needs.
  3. Audio file formats include: .mp3, .wav, m4a, and .wma.
  4. Video file formats are currently limited to .mp4
Therefore, it does not look to support Quantitative data such as the SPSS program.
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I have a plenty of qualitative data analyzed on deedose I would like to link with quantitative data collected through questionnars and not entered on deedose ( on the same project on migration and HIV)
Do you have any practical recommandations ? Thank you
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Dear Hancart Petitet Pascale,
Please analyses qualitative data and quantitative data separately. Corss check whether your qualitative data is supported by quantitative findings or vice versa.
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The supernatans will be used to analyze the cytokines present, using ELISA/Bioplex
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If I use heat inactivation, will my peptides (cytokines) be denaturated?
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We have seen whats app messages in India since 2014 regarding the HIV virus transmission through a fruit drink called Mazza- as one of the employee was HIV positive and had cut on his hands while packing the mazza in company when his blood was spilled to the juice before packed and any pack of the Mazza made in 2014 may contain the virus ad avoid drink the Mazza'' is the message circulating i the whats app.. now the question is do the viruses like HIV, HBV, HCV or HSV survive in this type of juices as it contains the moisture, and virus contaminated blood cells will remain viable and get transmitted to any one who consume it? This is not only the case but there are stories about the transmission through fruits like Pine apple, Water melon, Banana etc.. as a bio terrorism activities.. it is a duty of any one who belongs to this science society to make all the layman clear about the survival ability and transmission of those viruses to avoid such messages or to take care of themselves..i have many things to say here but want all your scientific opinion or suggestions for the society...
Karuppasamy Pandiyan..
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Hi, HIV is transmitted via body fluids especially blood of infected patients to a human subjects in contact with the body fluids of the infected patient provided the receptors for the establishments are there. AIDS spreads through body fluids(eg. Blood or semen). It can't spread by air or food.
The Centre for Disease Control(CDC) states that the HIV virus can't survive long outside the human body. And if by chance ingested(by consumption of infected blood and not through food - hypothetical situation), it would be destroyed by the digestive juices (HCl in the stomach).
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We are trying to quantify HIV RNA copies/ml by RT-qPCR. However, we only have a DNA plasmid containing our sequence of interest to use as a standard right now. We are extracting the RNA from dried blood spots. Our samples are limited and contain very low copy numbers so we can't use any of those for a control.
Thanks in advance!
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what's the primer and secondary antibody to use in western blott method to determine the activity of immunoglobulin yolk (IgY) as anti HIV which produced in chicken?
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Siti: A cleaner (better) way to do your WB is to purify your anti-HIV primary antibody (IgY) from the antiserum, and conjugate directly to HRP. We've used this approach in other antibodies (IgG) in the same way and obtained beautiful results (single band in most cases. Check out my RG account.
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Please I need recent studies on interferon-gamma, interleukins 6,10 and hepcidin in pulmonary tuberculosis patients co infected with HIV infection.
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Thank you.
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I am planing to start a project on HIV exposed uninfected adults so you work is of interest.
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I have published a coup´le of papers on HIV-exposed uninfected children many years ago, but really the best idea is to search through PubMed the terms "HIV-exposed uninfected", and you´ll likely get a lot of recent works on the subject.
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I mutated the U3 region in one subcloning and am trying to add it to wildtype R and U5 regions of HIV-1. To do this, I added an 8 base pair restriction site between U3 and R in order to get it into the same plasmid. I am wondering, would this 8 base pair restriction site have an affect on the overall function of the LTR? I am cloning this all upstream of a reporter gene to see what affects mutations in just the U3 region have on the promoter of the virus. But I am wondering if this 8 bp insertion has any impact of its own? Please and thank you.
EDIT: I do not want any effect from the insertion of the restriction site. I just do not know any other way to combine the mutated U3 region to the wildtype R and U5 regions without the introduction of restriction sites using primers and PCR. I am just wondering if doing so somehow affects the function of the LTR as well? And whether since it is an 8 bp site rather than a 6 bp site for example, that it would have any other impact due to reading frames etc?
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We did similar modifications of the foamy virus LTR and observed a dramatic decrease of transcriptional activity. I would assume the HIV is, due to TAR, even more affected. I would suggest to use overlapping PCR or Gibson cloning to fuse fragments in the LTR.
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is there any specific sure site? or random?
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Dear Debashis Dutta;
I share the same idea than Emmanuel. At the chromosomal level, HIV integration is strongly favored by the presence of the cellular factor LEDGF / p75. HIV IN binds to the cellular factor LEDGF/p75, which promotes efficient infection and tethers IN to favored target sites. The HIV integration machinery must also interact with many additional host factors during infection, including nuclear trafficking and pore proteins during nuclear entry, histones during initial target capture, and DNA repair proteins during completion of the DNA joining steps. Thereby, try to see if this cellular factor LEDGF / p75 is found in all chromosomes and I think that you will have an answer to your question.
Marcellin.
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Hi i need to establis a infection model of dendritic cell but at the same time i need infected cells don't produce the virus. Exists a HIV strain that meets this criterias? Or how do you suggest i can achive this result?
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I need to analize the effect of hiv genome integration. And i need this strain is the more similar to wild type. But i don't want this cells produce viral particles.
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Standard precautions are meant to reduce the risk of transmission of bloodborne and other pathogens from both recognized and unrecognized sources. (WHO) It is also recommended to assume that every person is potentially infected or colonized with an organism that could be transmitted in the health-care setting and apply the following infection control practices during the delivery of health care. (Guideline recommendation). Personal Protective equipment are to be used as one such measure. But I am unable to find whether the OT table and floor should also be covered with plastic? Please give your opinion with logic (reasoning) and evidences.
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The built environment should be appropriate to allow cleaning and disinfection e.g. Impervious and intact surfaces for floors , walls , coverings on the mattresses, that allow ease of cleaning and prevent ingress. The principles of environmental decontamention after any patient is based on cleaning then disinfection if needed Including after spillage of blood or body fluids or patient known to be infected e.g. MRSA! CPE etc . All medical devices which includes the theatre table and any device used for treatment and therapy must be provided with manufacturer instructions for decontamination which must include method, product for risk levels of contamination low, medium, high risk!. In the UK, decontamination is guided by medical devices directives and Health technical memorandum's on decon. There are also national standards for environmental cleanliness and infection control in the built environment guidance to refer to. Therefore plastic covering for floor and table is not needed as the environment should be appropriate to prevent infection and allow decontaminationalongside management and decontamination of equipment and medical devices.
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do HIV exposed dogs qualify for PEP
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Dear Mondo, HIV cannot infect dog.
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The answers of the above questions may be
1. Raido
2. TV
3. Newspaper
4. Book
5. Friends
If someone reply more than one answer then how can u analyze by using spss? How can i make questionnaire in spss?
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Answer
Hello Aitawari,
As Eugene Bogodistov indicates, you may use SPSS to analyze such questions. The key is to use the "Multiple Response" option to declare a set of related responses as a group. Here's an example, using your categories.
Variables for one such question had been defined as (with the instruction, "Check all that apply" ):
V01a was Radio (0 = no, 1 = yes)
V01b was TV (0 = no, 1 = yes)
V01c was Newspaper (0 = no, 1 = yes)
V01d was Book (0 = no, 1 = yes)
V01e was Friends (0 = no, 1 = yes)
Here's a sample data set for the variables:
v01a v01b v01c v01d v01e
1 0 1 0 1
0 0 0 1 0
1 1 0 0 0
1 1 0 1 0
0 0 1 1 1
0 0 1 0 1
Here's syntax that will declare and report the set as a multiple response group:
MULT RESPONSE GROUPS=$V1_set 'Where did you hear about us?' (v01a v01b v01c v01d v01e (1))
/FREQUENCIES=$V1_set.
The report is shown on the uploaded page.
Good luck with your work!