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.
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I am interested in calculating the HIV proviral load from the host genomic DNA using a house-keeping gene. What would be the best way for quantification without using a standard DNA template concentration?
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Question needs more clarification. But I believe this may be achievable using digital PCR.
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I'm cloning HIV SOSIP protein into expression vector p818 but I can't find any complete sequence of the vector. Does anyone have it?
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It's the vector our other SOSIP sequences are in (that I'm trying to clone my own protein into) but we don't seem to have a complete vector sequence anywhere. I was hoping to double check my digest cut sites
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I am proposing to research about continuous utilisation of HIV care and it's challenges and strategies that PLHIV use to engage in care. I was hoping that i would use SCT to relate my variables but it's failing to come out well.
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Dear Victoria Tumusiime
yes . social cognitive theory make a good model to study continuous utilisation of chronic care.
you can also employed ( social learning theory ). for more information you can follow my article( Challenges impede AIDS patients in Jordan to integrate them into society.)
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Hello,
I have a data of a retrospective study and one of the variables is the measurement of HIV viral load in patients. The data is not normally distributed according to Shapiro–Wilk test of normality and Kolmogorov–Smirnov tests of normality.
So, I am using Median (IQR). The problem is that these values are equal to zero (most patients had viral load of zero).
My question: Is it ok to write median and IQR to have zero value? Or should I use median and SD?
If I use median and SD, then I should use parametric tests, right?
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No viral load is qualitatively different to amount of viral load, since zero really isn't an amount. So the concept of mean viral load is only meaningful, I propose, in those who have any viral load.
I would report the proportion who had no viral load and then, for those who had viral load, report median and IQR.
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Hey there,
I am working on cell-associated HIV RNA. Could someone please recommend articles related to extraction, quantification and diagnosis of intracellular HIV RNA or possible probes to specifically detect intracellular HIV RNA.
Thanks
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Please find related article
El-Diwany, R., Breitwieser, F. P., Soliman, M., Skaist, A. M., Srikrishna, G., Blankson, J. N., Ray, S. C., Wheelan, S. J., Thomas, D. L., & Balagopal, A. (2017). Intracellular HIV-1 RNA and CD4+ T-cell activation in patients starting antiretrovirals. AIDS (London, England), 31(10), 1405–1414. https://doi.org/10.1097/QAD.0000000000001480
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I am looking at HIV viral load in plasma samples from ART treated people living with HIV without using a commercial kit. As these samples are from virally suppressed individuals, they should have very low viral titre. I am looking for a good technique to concentrate plasma.
Thank you in advance for your feedback!
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Try dialysis. Dialysis | Sigma-Aldrich (sigmaaldrich.com)
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A strong Association has been described between Blood group O and Peptic ulcer, Blood group AB and Carcinoma cervix, Blood group A and Gastric Carcinoma , Blood group B and Pemphigus and Seborrhoric Dermatitis.
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What are some unanswered research questions on the safety / efficiency / tolerability of antimalarials, majorly artemisinin based combination therapies, use among women who are HIV positive?
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Almost used retrovaridae therapies
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There is a study on the impact of HIV on mortality in patients with COVID-19 (Article link: https://www.thelancet.com/journals/lanhiv/article/PIIS2352-3018(20)30305-2/fulltext). According to Figure 3 of the article, the unadjusted impact of HIV on death risk was not significant, however the adjusted effect was significant. What could be the reason for this?
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Krishnan is right - while I think that any correlation with merely the diagnosis is not so relevant (since fortunately with early initiation of ART people living with HIV surely have a near normal immune system etc) - statistically adjustment for different factors in a cohort can go either way - positive and negative for respective factors. Do not think this study is to helpful to understand what is going on - also outdated (2021 paper)
authors write...:
"For similar reasons, we were unable to include data on antiretroviral therapy use, viral suppression, CD4 count, or previous AIDS-defining illnesses likely to be captured only in specialist care, so it was not possible to stratify results or quantify how much of the increased risk was driven by the minority of individuals with poorly controlled HIV. "
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The states (S) are V -vulnerable people as S1, S2 Rate of people with HIV diagnosis, S3 rate of people with AIDS diagnosis, S4 Rate of deaths from HIV/AIDS virus
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One of my own algorithms does that. It is called Discrete Probability Detector (DPD). DPD transforms any sequence of symbols into a transition matrix. Please look at the project:
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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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Hello , I am not sure, but check this video link, it may help you find a better answer.
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Is there any site or anynone here where i can get In house real PCR Protocols for HIV DNA diagnosis, HPV, HBV viral load, HIV viral load, Breast cancer and lymphoma PCRs
Thanks
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hello, first of all for any one who is at risk, education is very important, this video on youtube may help get a better vision:
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We need help using the MinIon sequencer for HIV samples that we are collecting...
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you can extract the RNA from those samples and generate corresponding library then sequence them with MinIon. MinIon offers the whole solution for that.
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My lab is working with primary cells from the patient and we would like to check if our cells are infected with HIV, HBV, HCV, etc by PCR. We would like to know how many cells do we need for this. The thing is that we don't have a lot of cells so we would like to use as little as possible.
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depend on the lower limit of detection (LOD) of the PCR, the viral load, and the stage ( or clinical feature) of the patient
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Does anyone know a paper describing the absence of RNA encoding the pseudotyped envelope protein such as VSV-G or Spike from SARS CoV-2 in the pseudovirus particles? I am troubled by the request from recombinant DNA committee to prove it. Thank you so much.
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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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I don't know alot about the subject, but couldn't RNA from the HIV virus be used to make an mRNA or viral vector vaccine similar to the covid-19 vaccine?
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I am looking for studies on the effectiveness nof the use of CBT and anxiety with people living with HIV.
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Its effectiveness is more than proven, in addition to being the Psychotherapeutic Techniques of choice in these cases. To see Literature in this regard, I suggest that you review several contributions on the subject that are posted here in "RG" (articles, books, monographs, papers, etc), in addition you can review the Bibliographic References that are provided; eg: "Interdisciplinary analysis of HIV / AIDS: Monograph" ("Análisis Interdisciplinario sobre el VIH/SIDA: Monografía", with a Chapter on its Psychosocial Aspects and another on "ad hoc" Psychological Intervention.
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in HIV / AIDS research, Could fecal microbiota transplantation be considered as an alternative therapy to antiretrovirals?
What treatment (FMT and ART) for people with HIV do you think is the most appropriate?
If the FMT has been around for many years, why do you think it has not been implemented as yet another alternative against HIV?
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No.
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Dear Scientists,
People who have lived with HIV for a long period of time. It seems dying of cancer now days. Are it Antiroviral drugs causing cancer? In 1990s, they were dying of typhoid because their immunity got destroyed. We are fighting HIV now cancer comes in. I was inquiring on issue since it is concerned with life. Thanks Bruce
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Thank you Dr. Ochomo for your contribution.
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We have been making viruses using HIV packaging system for years in our lab. We use 3rd generation system and make virus in 293T cells. We have been adding specific mutations to envelope proteins and one particular version of the envelope protein is not expressed well in virions (used a western to confirm) , whereas p24 levels (WB) and RT assay show comparable titer to wild type envelope protein. Any ideas if it is the cells or the mutations in the envelope affecting the envelope protein expression in virions?
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Hi Dr. Jyothi,
Could you elaborate a bit more?
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I'm looking for the genetic sequence for the TAR region of HIV.
If I put Transactivator Response Region, and HIV, and "genetic sequence: into a browser...is it not unreasonable to expect to be directed to a site that contains genetic sequence information for that element of HIV?
I'm looking for a reliable source of sequence information. I've exhausted myself going through NCBI...the above search query turns up "tat" and some homo sapiens genes...BUT NOT THE INFO I NEED.
PLEASE ADVISE.
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Hello Malik!
Thank you...but I'm actually looking for the sequence of the Transactivator-Response Region, not the sequence for the transactivator (tat). Malik Sallam
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The Nancy Padian study, (held in California from 1985 to 1997), was the longest and most comprensive study on transmission of HIV (or transmission of sero-positive-ness) between hetero-sexual partners in couples, who were 'assymetric', (one partner was sero-positive, the other wasn't).
In the abstract of the study one can read that the chances of HIV transmission were as following:
- Male to female: about 1 in 1,000 (more exactly 0.9 in 1,000)
- Female to male: +- 8 times less probable, so about 1 in 8,000 (or more exactly 1 in 7,200)
Hence, apparently during the whole period of 10 years of trial, it is said that "no" sero-conversions took place.
My question is: can anyone please shine a ligh on this..?
.
The study itself can be found here, (the full text in 'pdf file', is accessable with a link at the bottom of the article's abstract): " Academic.oup.com/aje/article/146/4/350/60711 " (copy & paste this link to the abstract, into your browser).
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Heterosexual transmission of HIV appears to occur with low frequency; however, the per-act risk of transmission depends on other factors that might increase the risk (e.g. STD, lack of male circumcision, etc.)
You can find the following
  • Estimating per-act HIV transmission risk: a systematic review (doi: 10.1097/QAD.0000000000000298)
  • Factors Associated with HIV Infection in Married or Cohabitating Couples in Kenya: Results from a Nationally Representative Study (doi: 10.1371/journal.pone.0017842)
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I'm tired of trying to get this information from NCBI. I put "HIV p6" or "GAL4-BD" into the search bar in NCBI (all databases), and expect to find a link to the sequence data...but no. These are pretty well characterized genes. I also tried "TAR" and "Transactivator Responsive Region" and get a list of links, the first one of which is for HIV's tat gene, and none of which have anything to do with the TAR sequence.
Anyone else have this problem?
Can anyone recommend a good source of sequence data? I want to input the name of a regulatory sequence or coding region, and actually get that information.
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Can HIV drugs will be a provisional or recurring option against COVID-19?
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May be
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Give me perspective, sample or studies that have been done before. Thank you so much
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Coping with a disease always includes our cultural beliefs and values.
Psychoneuroimmunology (PNI) and neurotheology are research fields that deal with the psycho-medical impacts on our body as living organism, which is highly informed by our mentalizations of a body state.
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What would be the mRNA-based vaccine's long-term effect if someone is infected with retroviruses like HIV? Can it make cDNA and integrate with the genome, or the mRNA is too low and too quick?
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Most vertebrates have hundreds of endogenous retroviruses in their genomes. Almost none of the endogenous retroviruses are fully functional and able to produce infectious viral particles, but many of them have potentially functional reverse transcriptase genes. Despite this, the revere transcription of messenger RNA to DNA and integration of that DNA into the host chromosomes is an extremely rate event. Vertebrate genomes do contain some pseudogenes which are reverse transcribed copies of messenger RNA, but not a lot of them considering hundreds of millions of years these genomes have been evolving.
There is more to reverse transcription and integration of DNA into genomes, than just having an RNA and a revers transcriptase enzyme in a cell. For one thing there needs to be a primer to start the reverse transcription process. HIV-1 for example uses the host cell lysine transfer RNA as a primer and HIV-1 has a region that is complementary to the lysine tRNA to allow this to happen.
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Can the formation of drugs against coronavirus also be useful against the Influenzas virus or HIV? This is because these viruses shared many common proteases for viral replication.
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Dear Talha Bin Emran, the answer is no, the targets and the mechanisms of action aren't the same. My Regards
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My question is related with the probability of having crossed containation when using a same processing plataform (fully automated) for viral load diagnosis of different kind of viruses.
Ex: can i process HIV, Sars-CoV2 and cytomegalovirus on the same automated plataform without affecting the quality of my results for each case?
Im really glad with your help.
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Christian, you can detect various viruses (SARS-CoV-2, HIV, CMV etc.) on the same automated platform, for either diagnostic or monitoring purposes. Molecular detection methods (I assume that your platform uses some kind of target amplification for viral load quantification, e.g. (RT)-qPCR, or isothermal amplification) are specific and properly validated methods should pose you no cross-detection problems with your various targets. It is already for some time that several commercial platforms enable the detection or viral load quantification for multiple viruses. Good laboratory practices should be used in order to properly identify samples (avoid mix-ups) and avoid cross-contamination between them, since these are the most common problems that lead to erroneous results in diagnostic lab settings.
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Immune activation and Viral load suppression in HIV patients
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Cure is a myth in cases of HIV . Yes the disease can be managed to keep pt healthy with good qol
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Combined drug therapy for HIV and TB
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Combined therepay for TB/HIV co-infection is effective, for a newly diagnosed HIV with TB, needs to start ant TB for the first 2 weeks, while assessing, IRIS, then we introduce ART based regimen, however remember to effect of rifampicin to DTG, we need to double the dose of DTG, as far as TLD based regimen is concerned, as this medication lowers the level of rifampisin, therefore, be cautius while administer TB drugs with the ART, know the issue of drug-drug interaction, thank you
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Hi, 
I know it is well accepted that only a fraction of produced HIV particles are infectious but I was wondering if anyone would have a good reference describing that contrast in virus culture supernatant (NOT plasma, as in plasma many other factors can interfere).
Thanks!
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In general, you can assume that only 2% of HIV viral particles are infectious for primary cells. Of course, this value can depend on the clone of HIV you're dealing with, for example, gp120 of R5-clones able to infect macrophages (eg. BaL, ADA) have high affinities to CD4 than primary ones.
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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 Anand Sonawane. We have tried it and it was working. However, long amplicons were not amplifying with this.
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With the help of the antibody level in the plasma, we can predict the presence of diseases such as HIV or other viral diseases with ELISA tests. (if there is a miswording in definition please inform- I am actually a beginner in studying immunology) I was wondering, '' Are there any other tests except ELISA to evaluate the presence of such diseases'' - based on antibody level in fluids taken from patients.
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EIA, Immunoflourescence , I recommend most modern assays.
But ELISA gives you higher accuracy, precision,specificity and sensitivity !!
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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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The lockdown can be eased out but with some restrictions in place. The lockdown can be lifted in some sectors and with some restrictions in place in some sectors. The sectors where lockdown will be lifted..the people should be made to follow preventive measures including wearing of mask, social distancing and avoiding unnecessary coming out of houses. As the cases may decrease,then the lockdown can be lifted completely. The travel should be banned from outside the countries or states for time being.
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Why has it taken too long to develop a vaccine that prevent transmit of HIV between opposite mature sex partners [man-to woman or vice versa] which humanity has accepted to live with and been adapted and now in a rush to develop a vaccine for COVID-19?
COVID-19, being in the family of SARs, Ebola etc for which a vaccine is available, why not enhance early/prioritize discovery and development of vaccines as a form of emergence preparedness?
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Active immunity is longer and stronger than passive immunity caused by vaccines and plasma convalescence. The vaccine will last one season. It will need to be done every year as with seasonal flu.
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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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For the first question: Yes, comparing between the WT and knockout gene is the basic approach for testing gene effects.
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We will use a survey which contains close-ended questions.
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if you are simply looking at the level of knowledge of college students with regards to HIV then MEAN should be good enough.
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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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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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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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Hello Cecilia, it is definitely possible. From Los Alamos HIV sequence database website, go to search interface and from there you will find options for subtype and genomic region of interest. There are also options for more identifiers like sequence length, country, year etc if you find them useful. Good luck.
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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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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 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 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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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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Dear you can design the questionnaire and administer to the patient and get thier response in connection to employment.
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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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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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I am also looking for the book, if anyone gets the link of the book then please give me the link.
Thank you in advance
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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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