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Every year most people fall sick to viruses with severe to no symptoms as body fight against it and eventually the virus becomes inert but during this process it multiply. What would be a low/median/rate per human episode?

Once they are inert they are probably drained in the toilet forms compost and back into the atmosphere but still inert.

Do these inert viruses become active when coming in contact with host?

Some of these questions can help understand if there is s growing problem of viruses as population/hosts grows sndvss they multiply especially of inert becomes active.

Wondering what are your takes on the growing strengthd of the enemy which is not getting destroyed in most cases?

TLDR;

Viruses multiply faster than humans so the threats from viruses are growing higher? Can people fall sick to viruses more often than before as s general statistics.

Not too sure if this is the right sub to ask but I’ll give it a go.

As the title suggests; is Ebola/Marburg a reason to not travel to a country? There’s been only one death (Ebola in Uganda) should it be avoided to travel in that country/neighbouring countries? I know Rwanda was dealing with a couple of Marburg cases back in November.

Any suggestions? I just started reading spillover but it raises a whole set of questions that it probably answers later on the book but I’m just curious lol.

I love your expertise and appreciate reading your insights here.

I’m curious: which viruses scare you the most and why? Do you feel like being a virologist gives you a unique perspective on your own experience of illness, when it occurs?

Thanks in advance!

I’ve heard that SARS-CoV-2 is a full body virus and affects other areas of the body besides the respiratory system. I’ve also heard that influenza is just a respiratory virus. But doesn’t the flu also affect other areas of the body like the heart?

Why is COVID-19 given extra attention? Is it just less likely for the flu to affect other areas of the body compared to SARS-CoV-2 or SARS-CoV-2 have more severe symptoms?

Do some organisms for antiviral purposes allow virophages to be in the body to prevent viral infections?

I'd like to learn more. Please recommend similar books.

Google and WHO say there are around a few million undiscovered zoonotic pathogens, and doesn't list the total number of all on earth. However that number seems far too low considering the vast biodiversity of earth. How many undiscovered pathogens are there?

Hello,

I am a medical student who is aspiring to become a virologist specialising in bacteriophages. As the choice of choosing a country to do my specialty and live is crucial for me, as virologists or even researchers or people with knowledge about the field, which country would you suggest to move to where I will be able to establish an academic career?

I'm between

Norway Denmark Netherlands USA Switzerland

Thank you in advance

I've been doing some research on viruses and bacteria but I've run into something I've not been able to find an answer to in my online searches: Can a virus lie dormant in nature for an extended period of time?

For example, could a virus lie dormant in soil for years or even decades, then when the soil is cultivated be transferred into the plants then, in turn, into the humans eating the plants?

Unfortunately everything I've found so far talks about viruses lying dormant in the human body for years, not outside the body / in nature.

Also, can someone explain like I'm 5 about how virus treatment works? Does the treatment 'kill' the virus particles? Or how does it stop them?

Thanks!

I remember reading a study before. I think it was about a virus in an animal species being less severe in unhealthy animals. But I can't find that study now. Since viruses also need many minerals to multiply, could the disease be less severe in a person who is deficient in these minerals?

Hello! I'm not actually sure whether or not this belongs here, but I am writing a story, and one of the major settings involves a world that has been torn apart by a virus of some sort. I wanted to base it off of a real virus because I find that easiest to consider, but I wanted to know what viruses would be a good basis for such a story. I really liked learning about Ebola in biology, and was initially thinking about something like that, but I'm not sure how probable a large scale outbreak of that would be. Aside from the story part, I am actually interested in learning about viruses and how they can effectively societies. Thank you for taking the time to read this!

Hi! I am writing a near-future sci-fi novel, wherein a world power has engineered a virus as a last gamble to sway a war in their favor. This hypothetical virus would, if there is any sensible way for it to conceivably be done, target young people of working age more than any other age range, and perhaps even men disproportionately more than women. This way, they'd reason, it would cause military efforts in a nation infected with it to crumble, but without it being a risk so huge it would be likely to cause the downfall of the very world power spreading this virus. They would take as many preventative measures as possible, and carefully spread it in strategic locations.
For extra context, ideally, it would be something that can linger, and spread through aerial means at short distances, unless it encounters extreme temperatures or the like.

If there are ways to accomplish this, for example with a viral carrier specifically engineered to discern environmental factors, or through extremely specific genetic engineering of the virus itself, or anything else you can think of, do let me know. And feel very welcome and encouraged to speculate about any related topics, I am always eager to expand my purview and change any plot elements to reflect that. Thank you!

Can you disprove the following "the total number of randomized placebo controlled trials showing human to human transmission (for viruses) is zero"

Can you link me a study that would disprove that? I know someone who is very anti-science/medicine and they told me, no such study exists. I looked around and found studies on bacteria. It can be any virus. Please send a link. Has no such study ever been done before? Or tell me why this quoted statement is invalid?

I know someone who is rather anti-science. I want to show them a link

Sorry if this doesn't belong here.

Can one virus make another go away?

I'm writing an informative on a virus and I'm not sure which one I should research. So if anyone knows any that aren't as common and/or are interesting in some capacity, any suggestions would be helpful.

Why does influenza survive for up to 48 hour on fomites and rabies virus does not? They are both enveloped virus, what is the criteria that allows such disparity? One needs saliva and inactives after drying, the other does not! :D Thanks

Please be kind and respectful! I have done some pretty extensive non-academic research on risks associated with HSV (herpes simplex virus). The main subject of my inquiry is the binomial distribution (BD), and how well it fits for and represents HSV risk, given its characteristic of frequently multiple-day viral shedding episodes. Viral shedding is when the virus is active on the skin and can transmit, most often asymptomatic.

I have settled on the BD as a solid representation of risk. For the specific type and location of HSV I concern myself with, the average shedding rate is approximately 3% days of the year (Johnston). Over 32 days, the probability (P) of 7 days of shedding is 0.00003. (7 may seem arbitrary but it’s an episode length that consistently corresponds with a viral load at which transmission is likely). Yes, 0.003% chance is very low and should feel comfortable for me.

The concern I have is that shedding oftentimes occurs in episodes of consecutive days. In one simulation study (Schiffer) (simulation designed according to multiple reputable studies), 50% of all episodes were 1 day or less—I want to distinguish that it was 50% of distinct episodes, not 50% of any shedding days occurred as single day episodes, because I made that mistake. Example scenario, if total shedding days was 11 over a year, which is the average/year, and 4 episodes occurred, 2 episodes could be 1 day long, then a 2 day, then a 7 day.

The BD cannot take into account that apart from the 50% of episodes that are 1 day or less, episodes are more likely to consist of consecutive days. This had me feeling like its representation of risk wasn’t very meaningful and would be underestimating the actual. I was stressed when considering that within 1 week there could be a 7 day episode, and the BD says adding a day or a week or several increases P, but the episode still occurred in that 7 consecutive days period.

It took me some time to realize a.) it does account for outcomes of 7 consecutive days, although there are only 26 arrangements, and b.) more days—trials—increases P because there are so many more ways to arrange the successes. (I recognize shedding =/= transmission; success as in shedding occurred). This calmed me, until I considered that out of 3,365,856 total arrangements, the BD says only 26 are the consecutive days outcome, which yields a P that seems much too low for that arrangement outcome; and it treats each arrangement as equally likely.

My question is, given all these factors, what do you think about how well the binomial distribution represents the probability of shedding? How do I reconcile that the BD cannot account for the likelihood that episodes are multiple consecutive days?

I guess my thought is that although maybe inaccurately assigning P to different episode length arrangements, the BD still gives me a sound value for P of 7 total days shedding. And that over a year’s course a variety of different length episodes occur, so assuming the worst/focusing on the longest episode of the year isn’t rational. I recognize ultimately the super solid answers of my heart’s desire lol can only be given by a complex simulation for which I have neither the money nor connections.

If you’re curious to see frequency distributions of certain lengths of episodes, it gets complicated because I know of no study that has one for this HSV type, so I have done some extrapolation (none of which factors into any of this post’s content). 3.2% is for oral shedding that occurs in those that have genital HSV-1 (sounds false but that is what the study demonstrated) 2 years post infection; I adjusted for an additional 2 years to estimate 3%. (Sincerest apologies if this is a source of anxiety for anyone, I use mouthwash to handle this risk; happy to provide sources on its efficacy in viral reduction too.)

Did my best to condense. Thank you so much! I have posted this on statistics-related subreddits as well; I wanted to try my luck here to see what thoughts virology experts might have.

(If you’re curious about the rest of the “model,” I use a wonderful math AI, Thetawise, to calculate the likelihood of overlap between different lengths of shedding episodes with known encounters during which transmission was possible (if shedding were to have been happening)).

Johnston Schiffer

And can a virus mutate more than once? I know there are different strains due to mutations but can the same virus that mutates from one strain mutate to a different one before it multiplies?

Hi everyone!! Looking for some suggestions. I’m so obsessed with learning about viruses and how they work in the body- especially the cell/molecular interactions with the immune system. Let me know if yall have read any books and have suggestions!

Hi everyone,

I'm planning to create a tool called Pathogen Info Search Tool that lets users search for pathogens and get info on causes, symptoms, treatments, and prevention tips. It’s aimed at biology students and researchers.

Do you think something like this would be useful? Any features you’d want to see?

Thanks for your feedback!

This OTC med seems highly effective for Covid, but seems to be efficacious for most viral illnesses.

https://www.frontiersin.org/journals/drug-discovery/articles/10.3389/fddsv.2022.962988/full

I work in a lab studying norovirus. I infect human intestinal enteroid mono layers.

Method: I dilute the virus (purified from stool samples of patients in local hospitals) in culture media then incubate for an hour to bind the virus to the surface of the cells. I wash the cells with more media, then freeze one of the plates at -20 to stop all metabolic functions. Then I stick the second plate in the incubator for 23 hours to get the 24 hr time point. I then extract the RNA and do RTqPCR to quantify how much virus is present at each time point. After normalizing to the quantity per well, I take the log10 value of each well and compare the averages of each condition from 1 hpi and 24 hpi. If there is at lease a 0.5 log increase, that virus is considered to be a replicating virus

My problem: the binding (1hpi) is expected to be around 2-3 but my binding is high around 3-4 (log10 scale). The 24 hpi is either equal to the binding or lower in some conditions. The virus is obviously binding but it just doesn’t appear to be replicating. This would be a fine and dandy observation if I didn’t get the exact same viruses with the exact same conditions to infect literally last week, some of them with very strong replication. Also, our lab has a positive control virus that everyone can get to grow super easily and that didn’t grow for me either.

Is it too high MOI? Is it too low? Is there a chance I’m doing something to prevent the virus from replicating? All my cells looked normal before and after infection so it’s not like we have a cell culture issue that I can sus out. I’m presenting my data to my PI and I want to come prepared for when she inevitably asks, “What do you think is happening?” I literally do not know what’s wrong or why this is happening. This is my second experiment with the positive control that isn’t replicating as expected.

Please give me any insight or some papers to read on the topic that might be useful.

Hello there. Recently I was briefly introduced into vaccines on my virology course. I heard there that one of the possible risks for libe attenuated vaccines is that they may be able to recombinate with wild type virus and therefore be viral again. Is that correct or there are more details in that?

Layperson here wondering what the virology/ epidemiology communities are saying about this. I recall early 2020 when the only people squawking about it were my microbiology friends who were widely regarded as chicken littles. Thanks in advance for any informed thoughts!

As I understand it, coronaviruses are constantly undergoing reassortment in their reservoirs. Could that mean the original SARS is long lost in nature? After years of reassortment?

I wonder if the same is true for SARS-Cov-2 in that we will never find the virus in a reservoir in an identical state to the wuhan isolates but will find genomic pieces of it reasserted into other strains.

I am really interested in virology. A recent sexual health scare got me interested in herpes virus and I’m baffled by the lack of knowledge in the Australian medical system.

1. Why isn’t western blot offered at pathology, given the known high cross reactivity of both HSV subsets and other viruses in current serology?

2. What are the different types of serology available, excluding western blot?

3. Given the discovery of genetically different HSV strains, that they differ in virulence and their is the ability to be infected with multiple genetic strains of the same subset - why isn’t it genetically typed during testing?

4. Why is there such a disparity between what is in the medical literature and knowledge of both doctors and sexual health experts?

• I have had 3 doctors and a sexual health nurse tell me they have never heard of western blot or HSV 2 glycoprotein G- specific antibody test.

• When i asked about viral shredding rates, sample size and methodology of the most current study i was met with blank stares

Whilst interested in many scientific fields and enjoy reading medical journals and listening to virology podcasts, im essentially a layman and an idiot by academic standards - is it unrealistic to expect people in the medical field to possess a deeper level of knowledge and understanding then myself