Virology For Dummies

Virology For Dummies

As we continue to navigate the daily changes regarding our response to the COVID-19 pandemic, I have taken a moment to pause and reflect on the person I would like to see emerge on the other side of this.  One gift that has been presented to me - is time. While I am still working, many of the other day-to-day tasks and activities are on hold.  It is this time that has helped me to understand there are areas where I can gain more knowledge and try to help to my family, friends, and co-workers understand the finer points of the current pandemic. 

All too often, it is the seemingly miniscule pieces of information that can reframe a person’s perspective of a stressful or threatening situation.  It is also crucial that each of us takes every opportunity to bend ourselves before the world does to sharpen our response to difficult situations. I decided that I needed to improve my understanding of how a virus functions. Except, I needed to explain this to my family with normal words lol.

A virus is very small, mostly because they are not complete cells.  A virus is made up of genetic material and some proteins.  To say it very simply, a virus uses the host cell’s “supplies” and “machinery” to reproduce itself. Think of this like a flash drive for your computer. It can not replicate itself unless it has a computer (host).

The virus will remain dormant until it can hijack a specific host cell. Once it makes its way in, the first goal is to replicate. Hidden in a cell, the immune system may not notice this for a little while.

Alright Mike, what's the difference between a DNA and RNA Virus?

DNA viruses are made up of DNA and proteins (that’s it!), and the amount of DNA is much less than in a human cell. The host cell converts the DNA into RNA (transcription) and then the host cell’s ribosome converts the RNA into protein (translation). 

The nasty little DNA virus uses the host cell to replicate its DNA. Psh.. unreal.

This is the same process that a healthy cell would be doing naturally, only with the host DNA, not the virus DNA.  The viral DNA and proteins the host cell made are then assembled into more viruses.  The host cell bursts or the virus transports itself out of the cell, which allows it to spread to neighboring cells. Examples of DNA viruses are herpes and various poxviruses.

SARS-CoV-2 is an RNA virus.  An RNA virus enters the host with genetic material in the form of RNA and a special helper (reverse transcriptase for some if you’re curious).  SARS-CoV-2 has a unique protein spike on its surface which facilitates entry of the virus into the cell. 

The cell is once again hijacked, the only difference is that the RNA is incorporated into the host cell’s DNA using the reverse transcriptase.  This is not a super accurate process.  Small errors made at this point contribute to the high mutation rates seen with RNA viruses. 

Now, much like Cousin Eddie, they have made themselves right at home and use the host cell to complete their replication.  Another slight difference in SARS-CoV-2 is that it does not use reverse transcriptase but follows a similar process using the host cell.  Influenza, measles, and coronaviruses are just a few examples of RNA viruses familiar to us.


The next line of defense, if gratuitous hand washing and social distancing failed us, is our immune system.  We need to have a basic understanding of this in order to explain the testing related to SARS-CoV-2.  Our immune system makes antibodies (immunoglobulins) that are used to flag the antigens on the invading substance (i.e. like that protein spike we talked about on the surface of SARS-CoV-2). 

These flags then elicit an immune response from different types of immune cells.  This response is designed to limit viral replication and eliminate infected cells.  The two types of antibodies most important to understand testing are IgG and IgM.  IgM is first produced in response to the virus, while IgG is present toward the end when we have developed immunity. 

The second portion of this blog will discuss some basic concepts of testing for SARS-CoV-2.  Like myself, I am sure that many of you have heard about testing on the news with variable understanding of some of the core concepts.  Two types of tests in use are:

Polymerase Chain Reaction (PCR):Testing that is looking for the virus, like PCR, uses samples from nasal/throat swabs – and sample collection and can be quite unpleasant!  For PCR testing, the sample is prepared using special solvents to remove the proteins and to extract the RNA.  Now a special “cocktail” of enzymes is added to convert this to DNA.  This DNA is subjected to several heat cycles and if the DNA sequence matches a known sequence (i.e. the viral genetic sequence), there will be amplification of this DNA sequence and it will produce a “signal” as positive.  These heat cycles are performed 25, 30, even 40+ times to complete the test!  Perhaps this helps explain why it takes a while to get results!  Once the test is complete, quantified measurement of the viral load can occur.  Some tests are considered RT-PCR.  This means that they are “Real Time” and can give results after each heat cycle. 

Immunoassay:  This is qualitative (Positive or Negative) for the presence of IgG and IgM.  The primary type emerging is the cassette style, similar to a pregnancy test.  Blood is added to a well and moved along the cassette through capillary action.  This will create a positive or negative response for the control, IgG, and IgM windows.  These tests are often more convenient than PCR but are not generally as sensitive or specific. 


 PCR is looking for viral genetic material and can determine the amount of virus in the host or viral load, while the immunoassay is focused on antibodies and is looking for IgG or IgM made by the patient in response to infection.

 It is important to remember that many of these tests are still under emergency use authorizations from FDA, therefore, FDA approved data on sensitivity and specificity is generally not available.  As with any diagnostic test, the result can provide valuable information but is only a portion of a complete clinical picture.  The testing and treatments are constantly changing in response to this pandemic.  If you have any interest in the latest studies related to this please go to clinicaltrials.gov for complete up to date lists.  I hope that you have found this information to be helpful.  If you would like more information on these subjects as well as some treatment information and vaccine development, we have a link below to a recording I did with Vivian Cintron, Ph.D.  She has a great background in this field and was an absolute joy to talk with.  She will tell you more about herself in the beginning and we will take a deeper dive into these subjects and more.  This was a great  opportunity and I hope that you can enjoy it, too.  I have links to references throughout the blog.  I have also included a PDF with some information on current vaccines in development. Potential-Vaccines



Tyler Christifulli's COVID19 Advanced Directives

I have no doubt healthcare providers all over the world are conciously aware of every cough, scratchy throat, and body ache. Could this be it? Will I be laying prone in an ED bed texting with an SPO2 of 50%? As much as we try to follow the correct PPE procedures, social distance, and open doors with our elbows, the truth is, this virus is very contageous and our job puts us in front of the sickest people in our community. 

I decided to write out my desired treatment plan if I catch this crap. This is a combination of "best data" and personal opinion. Please realize that at this point there is no vaccine or strong evidence for treatment.

When will I get tested?

The testing criteria is different depending on your region. There appears to be a lower threshold for testing healthcare providers because of their exposure to immunosupressed patients. While this makes sense, I will not get tested unless I meet two of the following:

- Develop a temperature (>100.4 oral)

- Dyspnea w/o exertion

- Multiple B lines on ultrasound per intercostal space (yes I have my own).

- Increased weakness

If I test positive:

I will self-isolate in my basement. I have a Lumify ultrasound and pulse oximeter I can use to monitor my daily disease progression. I will only go to the hospital if my shortness of breath becomes apparent upon rest or my SPO2 drops below 90% . This is purely because I do not have an oxygen source to supplement room air or power a CPAP device.

If I test negative:

I will self-isolate in my basement and unfortunately be unable to help take care of the baby in the middle of the night ????????‍♂️. If you hear the drums - it's just me trying to loosen up the secretions.

Hospital Treatment:

Most likely I will present to my local tertiary facility that has yet to experience many COVID19 patients. There will be an inherit desire to intubate me if my pulse ox follows the normal course we have seen in case reports. The "happy hypoxemic" with a saturation of 50% and speaking in full sentences without anxiety. I imagine I will present as what currently is classfied as a "Type L" patient. This patient has:

Low elastance (good compliance)

Low lung weight (less edema)

Low V/Q ratio ( shunt due to atelectasis) 

Here is a great breakdown of Type L & Type H.

Why I do not want to be intubated due to hypoxemia:

SARS-CoV-2 attacks type two pneumocytes. This particular pneumocyte is responsible for releasing surfactant. I am pretty sure everyone has heard of surfactant, but this junk is seriously important. Surfactant reduces the surface tension between air and water. Water has a higher surface tension because hydrogen loves to bond together tightly at the surface. If we infect our type 2 pneumocytes we decrease surfactant production and increase the risk of collapsing alveoli (atelectasis). 

The longer the alveoli are collapsed, the harder it is to get them back... and keep them back. This will also depend on surfactant production within that region. It is reported that type L COVID19 patients respond very well to CPAP. Applying positive pressure to the alveoli will recruit lung units that have collapsed due to atelectasis. We recruit more lung by dropping our diaphragm with spontaneously generated negative pressure than we do with forced diaphragmatic displacement from positive pressure. This is precisely why I do not want to be intubated unless absolutely necessary. And when I say ABSOLUTELY NECESSARY, I mean mental status deterioration or signs of type two respiratory failure (failure to ventilate). My hypoxemia should be treated with CPAP and positional optimization of alveolar blood flow (proning)

If I need to be intubated:

I think it is important that my respiratory goals are made clear:

1. Do not aim for an SPO2 of 100%. In fact, If you can keep me >85% I will be happy. Once we maximize a patient on 100% FIO2, the next normal progression is to increase PEEP. Type L COVID19 patients typically have good compliance and typically are not reported to need PEEP's above 10 cmH2O. Instead of increasing my PEEP, I would like you to increase my inspiratory time. It was once thought that PEEP should be set 2cmh2O above the lower inflection point of a pressure volume curve.

In reality, recruitment carries on past the lower inflection point and optimal lung recruitment takes longer than a second. For these reasons, I ask that once you get to a PEEP of 10 cmh2O - put me in APRV (airway pressure release ventilation). For an excellent breakdown of this mode check out Brian Kings blog here.

2. I believe there is a role for surfactant administration to maintain recruitment. Exogenous surfactant administration in adults is not well studied and not a routine practice. However, if you want to test it out on someone, I will volunteer and Sam Ireland will pay for it. Study looking at exogenous surf in adults here.



In the early viral stage of COVID-19 there does not appear to be an indication to administer steroids. If there was a role for antiviral therapy (i.g.hydroxy-chloroquine, chloroquine, remdesivir) it would be early. The use of steroids may have a role during the adaptive immune phase as illustrated below. 

Illustration is orignally proposed by Hasan K. Siddiqi and recreated by FOAMfrat.

Like many infectious diesease progressions, it is rarely the initial viral response phase that is deadly - it's the body's immune response. Evidence interpretation for steroid use is lacking any statistical benefit, however the timing of when the steroid is administered is extremely salient. If given too early, immunosuppresion could increase viral replication. I am asking for steroids by day 5 - 10 of symptom onset if imaging and gases suggest worsening pulmonary condition and function.  This is covered by Josh Farkas in a recent blog here.


Coagulation Risk:

There is well documented evidence of thrombotic events in COVID19 patients. There appears to be risk factors that potentiate the prevelance of either deep vein macro-vascular thrombosis or pulmonary micro-vascular thrombosis. If my D-Dimer increases >1500 ng/ml, please consider giving me low molecular weight heparin (lovenox) if my renal function is normal. If my renal function sucks.. just start heparin. What evidence we have for this D-Dimer cut off is found here.


Sedation & Paralysis:

If I am placed on APRV I request that you avoid paralysis if at all possible. Precedex is my desired sedation drug. Initially I may need some fentanyl as my body adjusts to intubation. The benefit of APRV is to allow me to breath on top of the P high.  If my spontaenous effort is not communicating with the ventilator, I worry recruitment will remain sub-optimal. 



It seems obvious, but get me off the ventilator as soon as possible. As mentioned above, recruitment is best performed by conscious diaphragmatic retraction. Place the ventilator into a CPAP mode while I am intubated and evaluate my spontaenous effort. I will admit that this area of care is beyond my expertise and I will have to trust that my care provider will keep me on the ventilator as minimal as possible.


In reality, my care will be in the hands of the pheneomenal providers who dedicate their life to caring for others. This blog was a unique way of laying out a care plan with what little literature we have on the current pandemic. Would you ask for something different? How would you want to be treated? I look forward to your response.

References are hyperlinked throughout the article.


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