Quantum of cells directly infected by a virus?

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Discussion Overview

The discussion revolves around the nature of viral infections, specifically focusing on how viruses invade cells, the selection of target cells, and the quantification of infected cells. Participants explore the implications of viral load versus inflammation effects, and the potential methods for assessing the extent of viral infection in tissues.

Discussion Character

  • Exploratory
  • Technical explanation
  • Debate/contested

Main Points Raised

  • Some participants propose that viruses have specific cell surface requirements for infection, such as the ACE2 receptor for SARS-CoV-2, suggesting that not all cells with these receptors are necessarily infected.
  • Others argue that the infection process is random, leading to variability in symptoms among individuals, and that it is difficult to quantify the number of infected cells without invasive procedures like biopsies.
  • A participant mentions that the immune response, rather than the viral load alone, is often responsible for the symptoms experienced during infections.
  • There is a suggestion that while some viruses can integrate into host DNA and remain dormant, others cause immediate cytopathic effects, complicating the assessment of infection severity.
  • One participant expresses doubt about the feasibility of estimating the number of infected cells due to numerous variables involved in viral infections.

Areas of Agreement / Disagreement

Participants generally do not reach a consensus on whether viruses indiscriminately infect all cells with specific receptors or selectively target certain cells. The discussion remains unresolved regarding the quantification of infected cells and the relationship between viral load and inflammation effects.

Contextual Notes

Limitations include the complexity of viral interactions with host cells, the variability in individual immune responses, and the challenges in measuring infected cell counts accurately without invasive methods.

mktsgm
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TL;DR
Is it possible to quantize the number of tissue/cells directly infected or affected (cytolytic/cytopathic) by a virus?
In any viral infection, we know that an invading virus enters the cell and damages them (cytolytic/cytopathic). This may be a starting point for inflammation down the road.

Though initial inflammation may be beneficial, a longer than necessary inflammatory process proves more damaging than being useful.

What we see as the disease is the combined effects of the cytopathic effects of viral invasion as well as the effects of resultant inflammation.

1) If any tissue is invaded by a virus, does it invade and occupy all the cells indiscriminately, or do they select their dwellings?
2) Are there any symptoms associated with the viral load only minus the effects of inflammation?
3) If so, can we discriminate and differentiate between these two effects? Can we quantify and quantize just the cytopathic effects of the viral invasion only?
4) Also, if any tissue is invaded by a virus, does it invade and occupy all the cells, or do they select their dwellings? I mean, do they affect only a particular set of cells (in a tissue), and can we identify them?

All I want to know is, is there a method to their madness?
 
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No conscious method, purely passive.

Viruses have specific cell surface "requirements" to be able attack that cell. Example: SARS-Covid-2 only enters cells that have ACE2 receptor sites - arterial endothelial calls, alveolar cells are some of those with ACE2 receptor sites.

It is passive - the virus does not have any active control of where it wanders. The wandering virus in suffcient quantity can cause a localized inflammatory response. When there are a lot of them collected in a small area, like leaves blown by the wind into the corners of a wall yard, then macrophages and other immune cells may go into high gear. And do damage to nearby good cells, This is the cause of inflammation in or near tissues or fluids that do not have ACE2 receptor cells.

An extreme example MIGHT be MIS-C
Multisystem Inflammatory Syndrome in Children

https://emergency.cdc.gov/han/2020/han00432.asp
 
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jim mcnamara said:
Viruses have specific cell surface "requirements" to be able attack that cell. Example: SARS-Covid-2 only enters cells that have ACE2 receptor sites - arterial endothelial calls, alveolar cells are some of those with ACE2 receptor sites.

Thanks Jim..

My doubt centers around this. If SARS-Covid-2 is affiliated to ACE2 receptor sites, I want to know whether Sars-covid2 attacks 'all the cells' that have ACE2 receptors or only a select-few among them are attacked?

In other words, can we identify/quantify the number of cells that were attacked by the virus?
 
No. It is random, which my be why we see some people with few symptoms and some people with dire symptoms. We can guess that a particular organ or tissue is infected.
There is no way practical short of doing a biopsy and then trying to get a titer (sort of a count-like result) of virus, not a cell count of infected cells, from the tissue.

Plus I explained above that viruses can end up near infected tissues, so this further complicated things.

Also infected cells do not live long, they usually have their resources drained and then they burst.
 
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I doubt its possible to estimate the number of cells infected by a virus, there are just to many variables to consider. You have to think of infections as an interaction between the features of the organism and the features of the individual.
 
mktsgm said:
Summary:: Is it possible to quantize the number of tissue/cells directly infected or affected (cytolytic/cytopathic) by a virus?

1) If any tissue is invaded by a virus, does it invade and occupy all the cells indiscriminately, or do they select their dwellings?

Viruses infect cells that are physically accessible to them and are permissive (am I forgetting something here?) . These constraints restrict the type of cells a given virus can infect. There are lots of examples inThe Principles of Virology if you are genuinely interested in reading it.

mktsgm said:
2) Are there any symptoms associated with the viral load only minus the effects of inflammation?

According to my virology professor, the immune system causes most effects of sickness during common viral infections. For example, the cytokine storm during a flu infection is the reason your body feels like you've been hit by a truck. The flu viruses only infect cells in your respiratory tract and stays there because it does not move past the basal membrane. The sore throat you experience when you get sick, is the result of your immune cells destroying the tissue in your infected respiratory tract. SARS COVID-19 is similar because cytotoxic T cells destroy infected alveoli tissue which leads to fluid buildup and eventually death.

jim mcnamara said:
Also infected cells do not live long, they usually have their resources drained and then they burst.

There are many examples viruses that do not lyse cells of kill them after their replicative cycle. For example, the Herpes Simplex Virus integrates its genome into the DNA inside certain neurons and stay there for the life of the host. It stays dormant and replicates when the right cellular signals are present. Another example that comes to mind is the hepatitis B virus, which infects cells in the liver and recruits immune cells that kill infected cells and cause cirrhosis. There are countless viruses in every cubic centimeter of a healthy person's body. It's been estimated there are hundreds of trillions viruses inside of your body at any time. These viruses make up the human virome.

Source: The Principles of Virology
 

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