Science topic

Virus Diseases - Science topic

A general term for diseases produced by viruses.
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There is evidence that certain viral diseases (for instance, AIDS/HIV infection) decline our immunity and make us vulnerable to other diseases. Similarly, Does COVID-19 may have a negative impact on our immune strength against other diseases?
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COVID-19 infection alters immune and metabolic responses in patients, which together produce an inflammatory environment that is highly permissive to fungal infections.
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I'm looking for published or unpublished papers.
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Are there any reports on the correlation between the consumption of Cannabis and the incidence of immune system amplification in COVID -19 or any viral disease patients?
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Till date, there is no any report regarding the correlation between the consumption of Cannabis and the incidence of immune system amplification in COVID-19 patients.
Thanks!
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Many suspected cases of Corona virus are self or home quarantine , some of them may have difficulty in breathing and other symptoms but are still having negative report for coronavirus disease. So what should be the advice given by Physiotherapist to them.
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An Update for COVID-19 patients and their families - April 16, 2021, as follows:
"Caring for Someone Sick at Home" (USA Center for Disease Control website):
Advice for caregivers in non-healthcare settings
Updated Apr. 16, 2021
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If you are caring for someone with COVID-19 at home or in a non-healthcare setting, follow this advice to protect yourself and others. Learn what to do when someone has symptoms of COVID-19 or when someone has been diagnosed with the virus. This information also should be followed when caring for people who have tested positive but are not showing symptoms.
*Note: Older adults and people of any age with serious underlying medical conditions are at higher risk for developing more severe illness from COVID-19. People at higher risk of severe illness should call their doctor as soon as symptoms start.
Provide support
Help cover basic needs
📷
Make sure the person who is sick drinks a lot of fluids and rests
  • Help the person who is sick follow their doctor’s instructions for care and medicine.For most people, symptoms last a few days, and people usually feel better after a week.
  • See if over-the-counter medicines for fever help the person feel better.
  • Make sure the person who is sick drinks a lot of fluids and rests.
  • Help them with grocery shopping, filling prescriptions, and getting other items they may need. Consider having the items delivered through a delivery service, if possible.
  • Take care of their pet(s), and limit contact between the person who is sick and their pet(s) when possible.
Watch for warning signs
  • Have their doctor’s phone number on hand.
  • Use CDC’s self-checker tool to help you make decisions about seeking appropriate medical care.
  • Call their doctor if the person keeps getting sicker. Call local emergency service and tell them that the person has or might have COVID-19.
When to seek emergency medical attention
Look for emergency warning signs* for COVID-19. If someone is showing any of these signs, seek emergency medical care immediately:
  • Trouble breathing
  • Persistent pain or pressure in the chest
  • New confusion
  • Inability to wake or stay awake
  • Pale, gray, or blue-colored skin, lips, or nail beds, depending on skin tone
*This list is not all possible symptoms. Please call your medical provider for any other symptoms that are severe or concerning to you.
Call 911 or call ahead to your local emergency facility: Notify the operator that you are seeking care for someone who has or may have COVID-19.
Protect yourself
In This Section
  • Limit contact
  • Eat in separate areas
  • Avoid sharing personal items
  • When to wear a mask or gloves
  • Clean your hands often
  • Track your own health
Limit contact
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Keep a separate bedroom and bathroom for a person who is sick
COVID-19 spreads between people who are in close contact (within about 6 feet) through respiratory droplets, created when someone talks, coughs or sneezes. Staying away from others helps stop the spread of COVID-19.
The caregiver, when possible, should not be someone who is at higher risk for severe illness from COVID-19.
The person who is sick should isolate
The sick person should separate themselves from others in the home. Learn when and how to isolate.
  • If possible, have the person who is sick use a separate bedroom and bathroom. If possible, have the person who is sick stay in their own “sick room” or area and away from others. Try to stay at least 6 feet away from the sick person.
  • Shared space: If you have to share space, make sure the room has good air flow.Open the window to increase air circulation. Improving ventilation helps remove respiratory droplets from the air.
  • Avoid having visitors. Avoid having any unnecessary visitors, especially visits by people who are at higher risk for severe illness.
Caregivers should quarantine
Caregivers and anyone who has been in close contact with someone who has COVID-19 should stay home, except in limited circumstances. Learn when and how to quarantine.
When it's safe for a person who has been sick to be around others
Deciding when it is safe to be around others is different for different situations. Find out when someone who is sick can safely end home isolation.
Eat in separate rooms or areas
  • Stay separated: The person who is sick should eat (or be fed) in their room, if possible.
  • Wash dishes and utensils using gloves and hot water: Handle any dishes, cups/glasses, or silverware used by the person who is sick with gloves. Wash them with soap and hot water or in a dishwasher.
  • Clean hands after taking off gloves or handling used items.
Avoid sharing personal items
  • Do not share: Do not share dishes, cups/glasses, silverware, towels, bedding, or electronics (like a cell phone) with the person who is sick.
When to wear a mask or gloves
The person who is sick
  • The person who is sick should wear a mask when they are around other people at home and out (including before they enter a doctor’s office).
  • The mask helps prevent a person who is sick from spreading the virus to others. It keeps respiratory droplets contained and from reaching other people.
  • Masks should not be placed on young children under age 2, anyone who has trouble breathing, or is not able to remove the covering without help.
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Caregiver
  • Put on a mask and ask the sick person to put on a mask  before entering the room.
  • Wear gloves when you touch or have contact with the sick person’s blood, stool, or body fluids, such as saliva, mucus, vomit, and urine. Throw out gloves into a lined trash can and wash your hands right away.Practice everyday preventive actions to keep from getting sick:  wash your hands often; avoid touching your eyes, nose, and mouth; and frequently clean and disinfect surfaces.
Note: During the COVID-19 pandemic, medical grade masks are reserved for healthcare workers and some first responders.
Clean your hands often
  • Wash hands: Wash your hands often with soap and water for at least 20 seconds. Tell everyone in the home to do the same, especially after being near the person who is sick.
  • Hand sanitizer: If soap and water are not readily available, use a hand sanitizer that contains at least 60% alcohol. Cover all surfaces of your hands and rub them together until they feel dry.
  • Hands off: Avoid touching your eyes, nose, and mouth with unwashed hands.
  • Learn more about handwashing.
When and how to clean surfaces and objects
Cleaning with a household cleaner that contains soap or detergent reduces the amount of germs on surfaces and objects and decreases risk of infection from surfaces. In most situations, cleaning alone removes most virus particles on surfaces.
  • Clean high-touch surfaces and objects regularly (for example, daily or after each use) and after you have visitors in your home.
  • Focus on high-touch surfaces and objects (doorknobs, tables, handles, light switches, phones, remote controls, and countertops).
  • Clean other surfaces in your home when they are visibly dirty or as needed. Clean them more frequently if people in your household are more likely to get very sick from COVID-19. Disinfect if certain conditions apply.
  • Clean surfaces using a product suitable for each surface, following instructions on the product label.
When Someone Is Sick
If someone in your home is sick or someone who has COVID-19 has been in your home in the last 24 hours, clean and disinfect your home. Disinfecting removes germs and reduces their spread. See Caring for Someone Who Is Sick at Home for more information.
For more information on cleaning and disinfecting safely, see Cleaning and Disinfecting Your Home.
Track your own health
  • Caregivers should stay home and monitor their health for COVID-19 symptoms while caring for the person who is sick.Symptoms include fever, cough, and shortness of breath but other symptoms may be present as well. Trouble breathing is a more serious warning sign that you need medical attention.
  • Caregivers should continue to stay home after care is complete. Caregivers can leave their home 14 days after their last close contact with the person who is sick (based on the time it takes to develop illness), or 14 days after the person who is sick meets the criteria to end home isolation.
  • The best way to protect yourself and others is to stay home for 14 days if you think you’ve been exposed to someone who has COVID-19. Check your local health department’s website for information about options in your area to possibly shorten this quarantine period.
  • Use CDC’s self-checker tool to help you make decisions about seeking appropriate medical care."
  • www.cdc.gov/coronavirus/2019-ncov/if-you-are-sick/care-for-someone.html
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There are some viral diseases give you live long immunity while other not
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Depend
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Covid-19 vaccines are used for prevention of viral disease. If incidentally if any person got infected to coronavirus after vaccination then had vaccination has any affect on transmission of disease to others.
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Agreed with dear Chinaza Godswill Awuchi 
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The vaccination for COVID-19 has been started. Whether the vaccinated persons may left the precautions for controlling corona virus disease.
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The new analysis of the Oxford-AstraZeneca COVID-19 vaccine indicates that transmission of the SARS-CoV-2 from those who have been vaccinated could be substantially reduced.
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Previous research has suggested an involvement of meteorological conditions in the spread of droplet-mediated viral diseases, such as influenza. However, as for the recent novel coronavirus, few studies have discussed systematically about the role of daily weather in the epidemic transmission of the virus.
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viral diseases so bacterial diseases are so important especially in rural flocks.
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Fowl typhoid/pullorum disease (salmonella gallinarum, pullorum)
Fowl cholera (Pasteurella moltocida)
Collibacillosis (E. colli)
Mycoplasmosis (CRD, IS)
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As you all are familiar with the rolling updates on corona virus disease (COVID-19). Peoples are getting infected indicating exponentially growth- almost reached 1M today. What is your opinion regarding the vaccine that already has to be developed for the treatment of this disease ?
Don't you think we, the scientific community, are running for the popular science and number of citations only?
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Popular science research or problem solving research ??? I prefer the latter to the former.
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Coronavirus Disease (COVID-19) and Pregnant Women?
Kindly, could you support with recently accepted data?
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Gaber El-Saber Batiha I agree with Malangori Abdulgani Parande that there is still very limited data are available to come into an inference.
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Today the greatest threat on the planet Earth is the invasion by the tiny particle causing Corona Virus Disease (COVID-19). Most people infected with the COVID-19 virus usually experience mild to moderate respiratory illness and recover without requiring special and very advanced treatment. Older people and those having medical problems like cardiovascular disease, diabetes, chronic respiratory disease and cancer are more likely to develop serious illness.
The best way to prevent and slow down transmission is to be well informed about the COVID-19 virus, the disease it causes and how it spreads. One of the best practices to stay safe from infection is by washing hands or using an alcohol based rub (sanitizer) frequently without touching the face.
The COVID-19 virus spreads primarily through droplets of saliva or discharge from the nose when an infected person coughs or sneezes, so it is important to practice respiratory etiquette (for example, by coughing into a flexed elbow).
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What the exact mechanism of COVID-19 and why it's different from the other coronaviruses (MERS, SARS) in the same family?
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As per ayurveda there is strong relationships between seasonal change and immunity but experts want evidence.....As per my knowledge previous viral diseases specially pandemic has rapid spread during seasonal change.
And detoxification of body may play important role to control and prevent .
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An important factor, often not recognized, is that at the end of the winter season (so February / March on the northern hemosphere) our immune status and ability to overcome viral diseases is at its nadir. This is associated to or caused by the annual nadir in vitamin D status ( 25OH vit D3 ) as shown in the next publications
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It might induce immunosuppression.
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I am not fully aware of all investigators.
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Immunoglobulin is used to treat viral infection. There are different immunoglobulin already used for the treatment of different viral diseases. Whether immunoglobulin is available or not against the corona virus.
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Please take a look at this useful RG link.
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I've read one article about the Corona Virus Disease, that you can find in this link below
They've used DL method to " to extract COVID-19's graphical features and provide a clinical diagnosis ahead of the pathogenic test, thus saving critical time for disease control ".
Therefore, I found that it's interesting to get involved in such a study and try to get a solution for this disease.
Now, I'm looking forward to working with a group of researchers to discover this topic.
IF anyone is interested, please let me know so we can start right away!
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How can I purify infectious bronchitis virus from other viruses like Newcastle disease virus or Infectious laryngotracheitis virus?
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Are you talking about allantoic fluid or any other type of medium? The simplest try would be to treat with anti-NDV and anti-ILTV serum and pass through your biological system again. If NDV and/or ILTV are still detected, pass several times, each passage after treatment with antiserum.
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What are the data needed and exclusion criteria for the researches studying the prevalence of infectious diseases or viral infection incidence in epidemiological researches?
How to design the study and what are the suggestions to get a good questionnaire form?
Regards;
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Vaccines maybe different types. Ex: Vaccines may contain live viruses, inactivated or killed viruses. Among those vaccines, which would be the best option for animal viral diseases.
Thank you for your precious time!
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Inactivated or killed viruses by auto-claving. This vaccine is the right choose, which would be the best option for animal viral diseases. Vaccines contain live viruses are dangerous risk.
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We don't have any Reviewed sequence in Uniprot and no tertiary structure available for any of the protein of this Virus. How we can work on protein level?
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I suggest reading this recent article:
Hope it helps.
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the potential risk for Reye’s syndrome among children and teenagers when Infection with viral diseases and take Aspirin is taken as a hypothermia
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Reye’s syndrome is a rare, but extremely serious condition that affects children and teenagers recovering from viral illness such as the flu or chickenpox. It most commonly causes swelling of the brain and a large build up of fat in the liver. Rapid breathing, diarrhoea, continuous vomiting, irritable or aggressive behaviour excessive lethargy and decreased level of consciousness are some of the symptoms of Reye’s syndrome. The exact cause of Reye’s syndrome is not known, however links have been made between patients with an underlying fatty acid oxidation disorder and taking aspirin during viral infections. Please take a look at the following links for more details.
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As the strategies like Transgenics, Genome editing and topical application of dsRNAs by targeting viral/their vector genome are well known to manage plant viral diseases, I wonder which one among them is cost effective, safe, simple, accessible to all the farming community.
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Thanks Vincent
My concern is about using the technologies like transgenics and genome editing on which there are so many socio-economic & political hues and cries around the world. In this regard, I am looking for the comparative & analysed views of experts in the concerned field.
BASAVARAJ
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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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I am trying to find a new checklist of Iranian tick species and some information on ticks transmitting viral diseases, like CCHF. How many genera and species of ticks exist in Iran? Is there any complete references on these two topics?
Any suggestions and any related references would be greatly appreciated.
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Dear Mohamed,
Thank you so much for your kind support. I will be happy to receive any related papers on tick species and their importance in diseases transmission in your country, Saudi Arabia, and even Japan, if you access the literature.
Take care my friend,
Ali
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Usually we did HI test using NDV antigen (lentogenic strain) prepared by company. If we propagate this virus in ECEs it is approved to do HI test using the propagated strain instead of that obtained from company.
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Yes, you can, but you should use SPF ECE to avoid the existence of other haemagglutinating agents.
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I am preparing a recombinant Newcastle disease virus vaccine in fertile SPF eggs. I am going to test my vaccine candidate in guinea pigs. I want to remove egg proteins and concentrate the recombinant virus only to avoid any allergy or sensitivity in vaccinated animals.
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As far as I know, nothing you do will be perfect. It's unlikely your animals will have a reaction though.
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Future global threats to public health may come from one disease such as a new strain of avian influenza or from a combination of different disease outbreaks of both person-to-person and vector borne transmission. Whatever the causes are we prepared?
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I think Zika Virus
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Most of the invitro studies were performed on dengue virus serotype 2. Why this serotype is given more importance than the others?
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Hi Krishna Raja Muthuraman,
I am currently working with DENV, I will just share some of my thoughts. 
1. Since I am working in Singapore, local context is one of the reasons. DENV1 and DENV2 are the two major serotypes circulating in Singapore for the past ten years. The major circulating strain has switched from DENV1 to DENV2 since 2006. DENV3 is occasionally found, DENV4 is rare in Singapore. I am not very sure about other regions or country. 
2. It seems like DENV2 is the serotype that can well grow in mice compare to others. For the past few years, most of the animal model only using DENV2 as it can give viremia or other readouts. Only until recent years I think is 2016, the community has reported a DENV3 and DENV4 clinical isolate that can cause clinical manifestations and replicate well in immunocompromised mice. 
3. This is my personal guess, it might be because the marketed vaccine Dengvaxia has lower protective efficacy in DENV1 and DENV2 serotype, that is why more efforts have been invested in studying DENV2. 
Let me know if I said something wrong or illogical.  
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I am trying to inoculate healthy potatoes with PLRV and PVY using Myzus persicae as vector.
I came across a question where if I could let aphids obtain the viruses from excised leaflet by letting them feed on the leaves for their own appropriate acquisition time.
Can I create a leaf disk using those leaves, petri dish and filter paper and place aphids that went through starving period to make the aphids obtain transmissible viruses?
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Dear Jung-Wook Kho
 Longevity in vitro differ from virus to another
Yes you can, you may also try membrane feeding
you may visit my researchgate
Regards
Prof. Houda Kawas
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I am currently working on some in vivo studies. I need my influenza viruses, A/PR/8/34 (H1N1) and A/HK/8/68 (H3N2) to become adapted in mice (BALB/c). I am trying to generate the mouse adapted virus by lung serial passage. My procedure is as below:
1. Infect 2 mice intranasally, 29 uL in each nostril without anesthesia.
2. Incubate for 4 days.
3. Harvest the lungs of the mouse that showed most severe weight drop in 1.5 mL PBS.
4. Homogenized the lungs tissue, get the supernatant, filterd with 0.45 um filter and proceed to next passage.
Previously, after incubation, I harvest the lungs of both of the mice and pooled them together. However I realized it may not be appropriate as the mutation of virus in each mouse is independent; one might have adapted well and one may not but pooling them together and allow them to infect next mice, gene re-assortment between the adapted virus and non-adapted virus may occur and lead to a less virulence virus in next passage. ( I am not sure about this, it is my guess, I discuss with my co-researcher and he was agreed with me, and thats why current I am only selecting the mouse with most severe weight drop. I am having this speculation was because during one of the passage, one of the H1 infected mouse showed a very significant weight drop and symptoms at day 4 post-infection (>15 %) but when I pooled the lungs of the mice and proceed to subsequent passage, weight drop and symptoms of the mice in subsequent passage were not significant.)
Currently I am trying to only harvest the lungs of one of the mouse with greatest weight drop and proceed to subsequent passage. But no promising result is obtain. As a result, I hope that Prof. Racaniello can give me some advises. Is it correct for not pooling the lungs of the mice? It was also strange that the both the H1 and H3 viruses I obtained in each passage dose not show any HAU. (I am using 0.5 % chicken RBC). Present of the viruses in lungs and oropharyngeal were confirmed by PCR.
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Adaptation of pandemic H1N1 influenza viruses in mice.
Ilyushina NA1, Khalenkov AM, Seiler JP, Forrest HL, Bovin NV, Marjuki H, Barman S, Webster RG, Webby RJ.
 
Abstract
The molecular mechanism by which pandemic 2009 influenza A viruses were able to sufficiently adapt to humans is largely unknown. Subsequent human infections with novel H1N1 influenza viruses prompted an investigation of the molecular determinants of the host range and pathogenicity of pandemic influenza viruses in mammals. To address this problem, we assessed the genetic basis for increased virulence of A/CA/04/09 (H1N1) and A/TN/1-560/09 (H1N1) isolates, which are not lethal for mice, in a new mammalian host by promoting their mouse adaptation. The resulting mouse lung-adapted variants showed significantly enhanced growth characteristics in eggs, extended extrapulmonary tissue tropism, and pathogenicity in mice. All mouse-adapted viruses except A/TN/1-560/09-MA2 grew faster and to higher titers in cells than the original strains. We found that 10 amino acid changes in the ribonucleoprotein (RNP) complex (PB2 E158G/A, PA L295P, NP D101G, and NP H289Y) and hemagglutinin (HA) glycoprotein (K119N, G155E, S183P, R221K, and D222G) controlled enhanced mouse virulence of pandemic isolates. HA mutations acquired during adaptation affected viral receptor specificity by enhancing binding to alpha2,3 together with decreasing binding to alpha2,6 sialyl receptors. PB2 E158G/A and PA L295P amino acid substitutions were responsible for the significant enhancement of transcription and replication activity of the mouse-adapted H1N1 variants. Taken together, our findings suggest that changes optimizing receptor specificity and interaction of viral polymerase components with host cellular factors are the major mechanisms that contribute to the optimal competitive advantage of pandemic influenza viruses in mice. These modulators of virulence, therefore, may have been the driving components of early evolution, which paved the way for novel 2009 viruses in mammals.
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Importante buscar elementos para compreender melhor a situação que estamos vivendo na atualidade.
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There are differrent causes of Microcephally in general medicine...We need not to jump to write conclusion without proper investigations 
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Is shrimp white spot virus can also infect fish
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As far as I know it is not possible but molluscs (e.g. blue mussels, different oysters) can bear WSV and distribute it to crustaceans back. I don't know if those animals replicate the WSV.
Best wsihes
Sven
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I am in charge of Immuno-hematology Division at University of Kinshasa, Democratic Republic of Congo, in Africa.
This part of the World has high prevalence of hemoglobinopathies mainly, sick cell anemia, immunodeficiency disorders such as HIV/AIDS, thrombotic disorders, AML and ALL, and lymphomas due to high prevalence of variety of virus.
We are very limited in terms of genetics, molecular and chromosomic testings.
We would like to partner with an university / organization that can help us to build our capacity of providing  quality care to our many patients in terms of BM Transplantation services  
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Hi, on behalf of WBMT and WHO we wrote a paper dealing with this aspect. This is the paper:
Essential requirements for setting up a stem cell processing laboratory
T Leemhuis, D Padley, C Keever-Taylor, D Niederwieser,  T Teshima, F Lanza, C Chabannon, P Szabolcs, A, Bazarbachi, MBC Koh
Bone Marrow Transplantation 06/2014; 49(8). DOI:10.1038/bmt.2014.104
Best regards
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can zika virus be transmitted through sexual intercourse with someone carry the virus as the intermediate host?
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Dear Sir/Madam
Zika virus is a single-stranded RNA virus of the Flaviviridae family, genus Flavivirus. Zika virus is transmitted to humans primarily through the bite of an infected Aedes species mosquito. The mosquito vectors typically breed in domestic water-holding containers; they are aggressive daytime biters and feed both indoors and outdoors near dwellings. Nonhuman and human primates are likely the main reservoirs of the virus, and anthroponotic (human-to-vector-to-human) transmission occurs during outbreaks. Perinatal and possible sexual transmission has also been reported. Transfusion-associated transmission is possible as Zika virus RNA has been identified in asymptomatic blood donors during an ongoing outbreak (CDC info)..
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Validating first bleed  of rabbit immunised with plant virus . In this process, i am getting high background reading of more than 1.0 even with control i.e, Buffer.
Could anyone please let me know the reason for getting this  high background reading even in Buffer i.e >1 when i performed ELISA for diagnosis of virus infected plant samples. I Changed the coating buffer and rest of the chemicals and repeated ELISA but couldnt rectify the error. Where is it going wrong ?
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Sesha,
Evaluating the first test bleed of a polyclonal serum to a new antigen is often tricky because you are starting with several unknowns in terms of assay conditions and reagents. You probably do not have a positive control serum for comparison. In this case each step will require a negative control so you can distinguish specific antibody binding from non-specific or cross reaction binding.
Starting with the coating material, if you have purified virus it would be best to work out the assay conditions with this before using infected plant material.  If you don't have much purified virus then use non-infected plant material as a control. I assume you are ginding the plant material into some kind of coating buffer? You may have to test a dilution series of coating material, start wide with 1x and do serial dilutions of 1/10 dilutions out a few steps. Coating with a mixture such as this is tricky because there are so many other competing proteins, lectins, etc that can prevent sufficient amounts of your virus to bind.
For your rabbit serum it will also be best to look at a dilution series of your test bleed as compared to normal or pre-immune serum. Start at 1/100 or 1/300 and make serial dilutions of 1/3 into your blocking buffer (example: 3 ul serum into 300 ul buffer, mix, then 100ul of that dilution into 200 ul blocking buffer, mix, etc). Continue serial dilutions out to about 1/24,000 to start. You should get signal out beyond 1/2700 if you are getting an actual immune response to your protein. You may see that both the test bleed and control serum get high readings at 1/300 (or 1/500 in your case) but the control serum readings should drop off at higher dilutions while the test bleed readings stay high and drop off at a higher dilution. You may also see a "hook" affect and get higher readings of your test bleed at higher dilutions that then drop off eventually to background as it it diluted further. In this case your first dilution is too high and there is so much antibody trying to bind it is in effect blocking itself. If that happens you just start your first dilution at 1/1000 or so and dilute from there.
Lastly, you said your readings were high even with buffer alone. The comments made by others about the secondary (in your case Goat anti-Rb IgG) binding directly to your coating material are correct. If you add some goat serum (1% final) to your blocking buffer you can eliminate some of this background binding. The goat serum will contain goat antibodies that are unlabeled and will bind up or block the sites on your coating material. Later when you add the enzyme labeled Goat anti-rb secondary the only binding should be to your rabbit antibodies that are bound to your coated virus. The secondary concentration may also have to be titered out to make sure you aren't using it too concentrated. 
I hope these suggestions help!
Ellie
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Is there any relation established between viral infection and pain modulation?
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I think your question needs a little clarification. Viral infection is something that we can characterize precisely like we can know the quantity of viral particles, the interaction with other viruses...however the pain modulation is something really hard to characterize if not impossible. Seeing the previous answers, I think that the inflammation axe can be considered as promising but for me it is not sufficient alone.     
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Is it true that viruses don't have colors or our current methods are limited to detect it?
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Hej Sayed,
H1N1 appears in bright colours. See attached file. But whether avian flu does?
Best,
Guenther
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Zika virus (ZIKV) has attained worldwide attention due to its global concern and rapid pandemic potential. The World Health Organization (WHO) has declared it as a “Public Health Emergency of International Concern”. Though this virus was first isolated in 1947, its pandemic threat arises recently. The main mode of virus transmission is through mosquito (Aedes) vector. There are also other modes of virus transmission such as intrauterine, sexual and blood transfusion. Its linkage reflected for fetal anomalies and possible association with neurological disorders has crearted an alarming situation. Complete information on many aspects of this virus is yet to be available to the scientific community, which will help in designing better and effective prevention and control strategies to tackle this emergency. At present priority should be given to the mosquito control.
The whole world researchers are searching for a solution to stop its spread. Since the pathogenic potential of ZIKV is comparatively new, not much information is available regarding their genetic characterization which is most important in understanding - why the virus became virulent? What kind of mutation involved for its virulence? What are molecular differences between mosquito, mice and human adopted viruses?. The other area of interest is host-pathogen interaction studies which will provide the answers to how the viruses are crossing the placental barrier? Why it is causing microcephaly and or neurological disorders? Currently, there is no vaccine is available and scientists should focus on isolation and development of vaccine on war foot basis.  
We need to find out in details about its emergence and evolution, genetic and molecular characterization, epidemiology and timeline, current scenario, transmission and spread, clinical signs and pathology, pathogenesis, advances in diagnosis, surveillance and monitoring, vaccine development, prevention and control strategies, treatment and focus for exploring novel/emerging therapeutic regimens.
Our group of researchers recently reviewed its all salient literature available available in pubmed and compiled a very comprehensive review which is being published as a rapid communication , will be available by this March month end online (Information attached pl..)  
Zika Virus – Emergence, Evolution, Pathology, Diagnosis and Control: Current Global Scenario and Future Perspectives – A Comprehensive Review
Hence just thought to share some good information and updates with you all and also enrich myself with your knowledge and views / opinions.
The topic is now open for discussions by experts and public health officials for finding out a viable solution to save humanity from a big pandemiic?
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Google Engineers Are Trying To Help Fight the Zika Virus Outbreak
"A volunteer team of Google engineers, designers, and data scientists is helping UNICEF build a platform to process data from different sources (i.e., weather and travel patterns) in order to visualize potential outbreaks. Ultimately, the goal of this open source platform is to identify the risk of Zika transmission for different regions and help UNICEF, governments and NGO’s decide how and where to focus their time and resources. This set of tools is being prototyped for the Zika response, but will also be applicable to future emergencies..."
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I would like to know about the information of dengue virus serotypes. What is the different between four serotype; DEN1,DEN2,DEN3 and DEN4? 
Thank you :)
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The serotypes are, however, close enough that original antigenic sin applies. The existing antibodies to one serotype already exposed to are expanded, and the immune system accepts them as effective. But they don't bind well enough to eliminate the virus  as well as they should. The same is true for CD8 expansion. Consequently the disease can be severe after the first exposure.
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there was a patient with hepatitis B virus infection, proved by PCR detection of the virus,,,after 6 months the patient repeated the test by PCR and the result was negative ( no detection of virus) I requested Hbs antibody test and the result was negative,,,,
I am asking if there is possibility of the virus to be eliminated without Hbs antibody?
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Sorry, I do not know the answer to your question.
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Although PCR and NAH techniques proves that latent VZV exists in central ganglia, it cannot be isolated from human ganglia. What (camouflage) mechanism does the herpes VZV adopt to avoid detection in living humans? What is the mechanism of this "dormancy"?
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Thanks Dr. Thilo for your answer.
Well as you have mentioned, it is apparent that there are no virions produced in latent stage, and so no detectable mi RNA , but I assume it may be also due to the fact that the latent virion is too labile to be isolated. Also, there is evidence that the histone-associated virus genome assumes a circular episomal configuration and the lack of animal model makes it difficult to isolate the latent phase of VZV from the ganglia cells. However, there may be novel methods developed to isolate high titre cell-free viral extracts from the latent stage in future. 
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I am researching epidemiology of herpes zoster in Asia-Pacific, and so far have incidence data from Australia, Japan, New Zealand, Taiwan and Korea. The only data for Thailand is a rate of 0.26/1000 from Aunhachoke K, et al. Int J Dermatol 2011;50:428-35, which is much lower than other countries. I would greatly appreciate pointers to sources of any more data from Thailand, and also from Indonesia, Philippines, Malaysia, Singapore and India, if such exist.
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I found epidemiology data on herpes zoster in Thailand available from the Bureau of Epidemiology, Thailand, website at: www.boe.moph.go.th/boedb/surdata/disease.php?dcontent=old&ds=77
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The typical was a rapid spreading among the birds and a great mortality. In most of the birds the feathers in abdominal area were slightly removed. The youngest birds were not affected. The avian pox virus infection was excluded.
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Well, first of all i have to say that I'm more than happy to find this question and learned alot....
but in my experience it is a form of canary pox, as i have seen like it before and after vaccination the problem solved.
Unfortunately in my country 99% of the owners do not accept para-clinical  expenses so all we have are by examination.
and also most labs do not perform any testing unless for poultry and ornamental and pet birds do not get much of help.
I would be more than happy if you could inform me of your  Avian experiences...especially about canaries...
thanks
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I've been using the commercial Rotavirus ELISAs to detect murine adapted (EDIM and EC wild-type) strains of Rotavirus A, however their sensitivity for this application is quite low - though obviously they are perfectly fine for detecting human rotavirus A infection as viral shedding is so much greater than mice.
Does anyone know of a good sandwich ELISA antibody pair (viral capture and detection) that I can use to detect the relatively low shedding from adult mice? Ideally the detection antibody would be labelled with biotin or directly with HRP / AP.
Appreciate the help. 
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Please try sending message to ROTACLONE manufacturers. They might be able to help.
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We are trying to develop a biosensor to detect the Dengue virus (DENV) in field condition. Since DENV is an RNA virus, I need to design primers that can specifically bind to RNA. These primers are not for the purpose of any form of PCR but only to capture DENV.
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Hi Shishir.............. I believe you can use the same primers as we use for RT PCR to detect RNA in the field since DENV RNA lacks a poly A tail, we use its specific reverse primer for preparing the cDNA. You can take help from Anoop M et al., 2010; 2012.
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For example in HCV E1E2 region is hypervariable.
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Mutation rate and sequence diversity are two different things. On one hand you have the mutations which arise during replication in cells. These can occur more or less randomly (i.e. the mutation rate of the polymerase is more or less constant). However, these could in principle be influenced by the sequence context to yield hotspots or cold spots, and I am not sure if there is a lot of literature on where mutations fall within a particular genome (these need to be addressed in a system where selection doesn't act).
On the other hand, and I think what you are referring to, is sequence diversity in the virus after selection. Indeed, many mutations will be selected against, while in certain regions, such as the hypervariable regions of HCV or HIV, which are under immune selection, mutations will be selected for. So, the effects of selection skew the variability you observe in different regions, with regions that have beneficial mutations (such as immune selected regions) having higher variability.
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Both the vaccine and wild-type strains of measles can use SLAM / CD150 receptors. What exactly is responsible for loss of virulence of vaccine strain, if it has nothing to do with receptor usage? Any comments?
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Lymphatic tissues are primary targets for all Morbilliviruses. It is CD150 or SLAM, which is the original receptor for Morbilliviruses including Measles virus. The vaccine strains attenuated on Vero cell lines tend to use CD47 while they apparently have not lost ability to use the original CD150 receptor. Then what could be the reason for loss of virulence?
Immune stimulation along with immune suppression by two different pathways are well known phenomena.
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Is it safe to perform experimental infection of poultry with low pathogenicity avian influenza viruses (LPAIVs) in the absence of biosecurity level-3 (BSL-3) facilities? Do they they pose significant risk for humans?
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Hiii Zaheer
Its not safe to perform animal expts with LPAIVs without proper biosecurity. There is always chance of LPAI to mutate HPAIV. Due to genetic drift and shift, the virus is on regularly evolving itself to adapt host. so that its better to do animal expts in biosecurity level-3 (BSL-3) facilities
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Thanks Anand, I think your talk is quite reasonable
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I am analyzing the levels of secreted HBsAg in the hepg2.215 culture supernatant by commercial enzyme immunoassays (Monolisa™ HBs Ag ULTRA). My questions are:
1) Can i perform the test in a 96 well plate?
2) What is the incubation period required before taking the supernatant?
3) What is the minimum number of cells that can be used (seeded) in the well plate?
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We have been using the PLC/PRF-5 for doing the HBsAg immunoassays. We have observed a peak in HbsAg levels in the supernatant on day 4/5. This is ideally when we assay the cell free medium.
Just one question: Does any one have the HepG2.2.15 that can be shared with my lab?
Regards.
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Can a mosquito Aedes aegypti carry two different viruses (e. g. dengue virus and yellow fever virus)? and, could also transmit two viruses to a human with one bite?
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A. Aegyptii and other mosquitoes can of course carry two different flaviviruses. In fact overinfection with a second flavivirus is found quite often in nature. So theoretically at least, DENV and YFV could co-infect one A aegyptii individual at the same time. However, once in the mosquito body, progression of the infection of each of these viruses might affect the course of infection of the other. Different relationships can be possible: 1) mutual exclusion (a kind of competition) in which only one progresses, and the other fades away, 2) mutual enhancement, 3) no interaction at all The likelihood of a double infection being transmitted by a single bite depends on which type of interaction is established between both viruses in the mosquito body.
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I thought I could make CNDA and PCR portions of genome and sequence the PCR fragments but this isn't going as well as it should. Now I am trying to sub clone fragments and sequence - also not going well. I seem to be cloning much smaller fragments that I started with into TOPO XL. I am wondering if viral cDNA is a problem for my TOPO vector.
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We have done a considerable amount of sequencing of negative strand RNA viruses
The first approach provided the complete genome sequence for several novirhabdoviruses and vesiculoviruses of approximately 11,000 nt in length. The genome was divided into overlapping fragments of 500-600 nucleotides and these regions were amplified using conventional RT-PCR using RNA extracted from PEG precipitated (concentrated ) virus. In our hands the amplification of larger fragments, irrespective of the reverse transcriptase, is very inefficient and we always favour the shorter amplification products. In your case this may require 40 primer sets, but the amplifications can be easily achieved in duplicate on a single 96 well plate and the products sequenced directly using a single plate for the forward reactions and a second plate for the reverse reactions. The whole process can be done in a week or so. This process avoids any cloning issues.
The second approach we have used is 454 de novo sequencing using RNA from vesiculoviruses concentrated using a PEG precipitation in the same way. I can provide full details of the amplifications methods used up to the point of sending the sample for commercial sequencing if you wish. A 16th of a 454 sequencing plate was sufficient to obtain the complete genome, excluding the 3’ and 5’ termini sequences which were generated using standard 3’ and 5’ RACE procedures.
Finally, we are currently in the process of sequencing multiple genomes on a single plate using the equivalent of MID tagged primers, but we are still waiting for the data on this.
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is there any difference between replicon HCV cells and infected cells.. and what is it?
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Replicons are not able to produce infectious particles but are capable of RNA replication.
A minimal HCV replicon consists of the NS3 to NS5B nonstructural proteins flanked by the 5' and 3' viral NTRs. There can be a selection marker (neo, for example) and/or a reporter gene (luciferase, for example). See Lohmann et al, Science 1999;285:110.
There are HCV strains capable of a full infection cycle in cell culture (Huh7 is the most commonly used permissive cell line); most are based at least in part on the genotype 2a JFH-1 isolate. See Wakita et al, Nature Medicine 2005;11:791.