I’m starting an undergraduate research program at SPC, and my research focuses on how exposure to sublethal concentrations of commonly used disinfectants influences biofilm formation and antibiotic resistance in Streptococcus pneumoniae I’m transferring to UF in January 2026, and I would like to continue my research but with a virus similar to a filovirus, as my ultimate goal is to work in a BSL-4 lab to research filoviruses. What viruses could I use to transfer my research question that are similar enough to filoviruses?

So far I have VSV-EBOV (surrogate for filo), SARS-CoV-2, H1N1, Crimea-Congo Hemorrhagic fever virus, Rift Valley Fever Virus, Vaccinia Virus, and Hanta virus but I don't know if UF has any of these or if they can get them

It's known to be almost 100% in humans, and other mammals, but what about it's reservoirs species, bats?

Currently, there are three main plausible hypotheses that attempt to explain the origins of viruses. I want to know about other people's opinions on these hypotheses.

The Virus-First Hypothesis, which proposes that viruses predate cellular life. According to this hypothesis, viruses originated in the pre-cellular world, during a time when self-organizing molecular systems were evolving the ability to replicate themselves through ribozyme-mediated RNA autocatalysis. These early viruses may have existed before these molecular systems gave rise to protocells, which eventually evolved into the earliest forms of cellular life.

The Escape Hypothesis proposes that viruses originated from fragments of genetic material that “escaped” from the genomes of cellular organisms. These genetic elements evolved the ability to move between cells, infect them, and exploit their replication machinery to reproduce. This hypothesis mainly emphasizes that viruses emerged after the first cellular life forms, as they depend on cellular hosts for replication.

The Reduction (or Regressive) Hypothesis suggests that viruses evolved from more complex, free-living organisms that gradually adapted to a parasitic lifestyle. Over time, they lost the genes necessary for independent survival, as they became increasingly reliant on host cells for replication. As a result, viruses retain genetic material and some characteristics of life, but they lack the ability to maintain homeostasis or metabolize nutrients independently.

Each hypothesis has its strengths and limitations. What is your perspective? Which hypothesis do you find the most plausible?

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Only two new HIV cases were recorded among 2180 participants receiving LEN twice-yearly, compared to nine new cases among the 1087 participants receiving daily oral TDF/FTC (tenofovir disoproxil fumarate/emtricitabine). Lenacapavir demonstrated a 96% reduction in HIV incidence compared to background HIV incidence (2.37 per 100 person-years) and was 89% more effective than daily oral TDF/FTC in preventing HIV acquisition. 

Prep was consider 99.9% effective and there are almost none confirmed breakthrough cases. But lenacapavir already had 2 confirmed failure cases.

9 new cases out of 1087 participants in the prep group looks very high.

Am I missing anything?

Non-medically educated individual here - that finds virology fascinating. Have been reading about the history and origins of the herpies virus and a few medical journals here and there - have some questions.

Does being seropositive for any genus in Herpesviridae provide some level of protection against other genus?

Would purposely infecting people with simplex virus at its non preferred site (eg on the leg or foot) provide protection and reduce the severity of symptoms (if acquired) for people who were exposed the simplexvirus during sex?

• if yes, then why isn’t it done?

Are there different genetic strains of Human alphaherpesvirus 1? Does the alphaherpesvirus 1 mutate like covid?

Hi everybody! My partner and I are recovering from a nasty bout of a GI bug. I’ve sent a stool sample in to see if it’s actually noro, but the urgent care PA we saw suspects that it’s noro given our symptoms and the fact that there is currently an outbreak.

Assuming that it is noro, how long would you guys wait to see/visit family? And what precautions would you take when you’re there? We are supposed to head to our parents’ homes for the Christmas holidays next week and worried about spreading it to them.

We’d planned on seeing his parents one week after my symptoms first started, and five days after his. And we’re seeing mine 10 days after mine started, and 8 after his. So it will have been well outside the typical “48 hours after vomiting or diarrhea” window, but I also know that norovirus can be contagious for up to two weeks afterwards (and then another two weeks on surfaces??). Based on the research I’ve done, it seems like just seeing them is likely fine. What we’re wondering is how cautious to be about surfaces at that point. We can definitely hold off on preparing and sharing food until the full two weeks. But should we also be disinfecting the bathroom after use? And what about things like Christmas gifts and other things in our luggage — if we’re bringing them from our home, is there a chance those will carry the virus on them?

My parents both have chronic GI problems already, so I’m especially concerned about preventing them from getting it. Any advice would be so helpful!! TIA

“Of the 12 initial samples collected, 10 tested positive for malaria, although it’s possible that more than one disease is involved.

Further samples will be collected and tested to determine the exact cause or causes.”

https://www.who.int/director-general/speeches/detail/who-director-general-s-opening-remarks-at-the-media-briefing---10-december-2024

RNA-dependent RNA polymerase (RdRP), the enzyme responsible for replicating the genomes of RNA viruses and converting negative-sense RNA (3’ → 5’) to positive-sense RNA for viral protein synthesis, lacks the proofreading mechanisms present in DNA-dependent DNA polymerase (DdDP). As a result, errors (mutations) introduced during RNA replication are not efficiently corrected. This means that RNA viruses, such as the influenza virus, accumulate mutations at a much higher rate than viruses that carry DNA. These frequent mutations drive rapid evolution. Mutation creates variation, which will inevitably lead to certain strains with the ability to evade host immune responses and develop resistance to treatments.

Lyssavirus is like the Aussie rabies.

In a paragraph regarding interfering RNAs in use as protective mechanisms against viruses she says: “A similar but novel immune mechanism related to RNAi has recently come to light in archaea and bacteria helping them to combat phage attack. In this system, short gene segments from the invading phages are implemented into the host genome. These then code for RNAs which specifically bind to the invaders proteins and inhibit subsequent protein production, so aborting the infection before new viruses can be assembled”

I kinda read it as the phages genes are transcribed into RNA that actively inhibits the phages own protein production? Seemed pretty contradictory so I’m not sure if I misunderstood or it was just poorly worded by the author. Any help? :)

I was reading about the mechanism of action and it sounds like something that other viruses besides measles could cause. Essentially, the immune system targets measles infected lymphocytes for destruction and our immune memories are destroyed in the process

Following up on the news about the USDA mandate to test milk for bird flu (which will probably be overturned next month), we keep hearing that we're only one step away from human to human transmission. What are the odds of a pandemic on the scale of COVID (or greater) in, say, the next four years? I'm really hoping we don't have to live like that again anytime soon. I'm having an existential crisis right now. If anyone can reassure me/give me probabilities, that would be nice.

Hi, virology enthusiasts!

I'm working on a novel where a zombie virus plays a central role, and I've been brainstorming how to make it as scientifically plausible as possible. The virus I've designed borrows characteristics from existing pathogens, such as its modes of transmission and its effects on the brain and behavior. I’m aiming for a balance between creative fiction and scientific feasibility.

Here’s a brief summary of how the virus works:

Airborne transmission: Symptoms like coughing, fever, and delirium appear within a few days, and the virus eventually damages the brain’s amygdala and frontal lobe in most people. Some individuals, however, are immune to airborne transmission or can get sick via this route without experiencing brain damage.

Blood/saliva transmission: Leads to rapid brain damage within minutes, even in individuals who are resistant to airborne transmission.

Pheromone production: Post-brain damage, infected individuals emit pheromones that deter other infected individuals from attacking them.

Post-brain damage symptoms: Outcomes vary. Some die, while others exhibit uncontrollable rage and retain motor skills, effectively becoming “zombies.”

The virus’s origin in my story is linked to a fictional scenario involving AI-designed pathogens and improper lab protocols, so I’m not looking for clinical accuracy but more insight into whether my ideas align with general virology principles.

Would anyone here be willing to give me feedback on this concept? Or could you point me toward resources or individuals who might be interested in helping me refine the biological aspects of my virus?

Thanks in advance!

Hi folks,
a fresh Virology graduate in my family has requested some archival virology books for xmas. I am not a virologist and do not know where to start, but want to contribute to science vicariously. Figured I'd ask the community for recommendations. Any suggestions?

Hi. I'm a human biology student in Portugal and I was thinking about working with virology in the UK. Can I work there with a master's degree or do I need a doctor's degree? And what should I do to make that happen?

Hello all!

I did my PhD in Cell and Molecular Biology with a concentration in Virology in the USA. I have 5+ years of BSL3/4 flavivirus + SARS research experience and I am currently working as a Postdoctoral Fellow in a medical center but I would like to move to Europe/UK. I have heard a lot of praise of the work-life balance in the EU and honestly my PhD was super tiring as it usually is for everyone. If anyone has any tips on where and how to apply for scientist/research positions please let me know I would really appreciate it! Also, how easy is it for scientists to get sponsorship for such roles? TIA!!

Good afternoon everyone! Hope you’re all save and sound. Now I am actively trying to find literature on the prospects of creating vaccines against covid. I found articles about vaccines based on self-amplifying RNA (saRNA), as well as some information about the use of various TLR agonists for additional stimulation of immune response. So, if you have come across anything else interesting in this area, I would really appreciate a hint 😇. Thank you in advance!

I should clarify that this is not for actual/personal use.

I’m working on good practice report as part of my global health project. Part of it is coming up with a new strategy for addressing the health the problem.

I wanted to incorporate the use of dengue screening tests alongside fever screening in airports. The issue is I’m having difficulty finding information for “at home” dengue screening tests. There has been one test I was able to find but it only shows up in Amazon and I can’t find any manufacturing information about the test itself or much information on the company that produced it.

do you need a medical degree or phd or are there other routes into the career?

I have already done a lot of research on HPV infections and have read that the infection is eliminated in 9 out of 10 cases by the immune system.

But is the virus really completely eliminated in 9 out of 10 cases by the immune system or just temporarily inactivated?

Just asking, because I never have really been able to grasp the 50% CFR/IFR that H5N1 has had historically, and I believe that mild/asymptomatic cases were highly missed in many cases.