Note: This thread is related to #Coronavirus #COVID19

Follow the World Health Organization's instructions to reduce your risk of infection:

1/ Frequently clean hands by using alcohol-based hand rub or soap and water.

2/ When coughing and sneezing cover mouth and nose with flexed elbow or tissue - throw issue away immediately and wash hands.

3/ Avoid close contact with anyone that has fever and cough.

Prof Francois Balloux+ Your Authors @BallouxFrancois Director @UGI_at_UCL. Trying to do my bit to fight disinformation in the COVID-19 era, where every day feels like a Sunday with a nasty hangover. Jun. 30, 2020 2 min read + Your Authors

Over the last weeks, a substantial amount of new evidence has become available about immunity to #SARSCoV2. This information can be difficult to process and integrate. As such I felt it may be helpful to write a thread to summarise the information and provide some context.
(1/13)

The immune system is highly complex and comprises a series of different arms. Innate immunity represents mostly first-line responses with no memory of prior infections. Acquired immunity can be broken down into 'antibody-mediated' and 'T-cell-mediated' immunity.
(2/13)

Antibody-mediated (humeral) immunity is based on B‐lymphocytes that are reactivated to produce antibodies when exposed to a pathogen upon reinfection. Until recently, all the attention in the #SARSCoV2 debate has been on antibodies.
(3/13)

Antibodies are fairly easy to quantify which is the basis of serological tests that inform whether someone has been infected with #SARSCoV2. Though, it is becoming apparent that not everyone infected mounts detectable levels of antibodies.
(4/13)

Antibody levels to #SARSCoV2 also wane fairly fast, in line with other coronaviruses. As such, antibody tests can fail to detect prior infection in particular for asymptomatic or mild infections. Serological surveys may underestimate the proportion of people infected.
(5/13)

T-cell-mediated immunity against #SARSCoV2 has received little attention until recently. The main reasons are that T-cell response is less straightforward to measure and it is generally considered less important for vaccine efficacy.
(6/13)

T-cell response is a late immune response and does not generally make the host refractory to infection. As such, a vaccine blocking infection would need to elicit a strong antibody-mediated response.
(7/13)

Though, T-cell immunity is essential for controlling an infection and reducing symptoms. #SARSCoV2 seems to elicit robust T-cell response even in asymptomatic/mild patients. There is also evidence for widespread cross-immunity with 'common cold' coronaviruses.
(8/13)

There are four known coronaviruses (229E, NL63, OC43, and HKU1) that cause 15-30% of "common colds". They circulate primarily in young children. Most people get infected with one or more of these viruses at some point in their lives.
(9/13)

In contrast to antibody-mediated immunity, T-cell response is extremely long-lived. For example, people infected in 2003 with SARS-1 still mount an immune response to #SARSCoV2 17 years later.
(10/13)

While there is still no established case of #SARSCoV2 reinfection to date, it is likely those will be observed soon due to fairly fast waning antibodies. Though, anyone with a prior exposure to #SARSCoV2 is expected to experience far less severe symptoms upon reinfection.
(11/13)

Most 'hight-tech' vaccines tend to focus on eliciting narrow antibody responses. T-cell response works best against the whole viral diversity. This raises the question whether there should not be more efforts towards 'traditional' vaccines (i.e. attenuated/inactivated).
(12/13)

To finish on a lighter note, given how little we still know about the best-studied virus ever, it amuses me to no end that some believe it might have been cunningly engineered by nefarious boffins to target ethnic group X or Y, or behave in the way it does.
(13/13)


You can follow @BallouxFrancois.



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