Thread by @NjbBari3

Small study. 55 infants.
Estimating susceptible pool of infants to RSV reinfections.
43% reinfected.
Memory T cells found in only 38% of infants, and there was no difference in how many had this memory between those reinfected and not reinfected.

My conclusion. Past waves not a good predictor of future wave size or severity. Significant numbers of susceptible humans remain in the population. Any estimates of "immunity gap" must take into account a lack of durable immunity to RSV in infants.

Past experience note that younger infants have physiological reasons to suffer more severe disease. (small airway, soft chest walls). This must also be weighed when considering policy that can affect timing of exposure of infants to RSV.

nature.com/articles/pr200…

Further study is warranted with rigorous measurement of how many infants are infected on a population level scale and how this affects reinfections and disease severity in the first few years of life when infants are most at risk.

Further study is also warranted to measure exactly what children's immune systems are doing as they negotiate the new combinations of viral illness. RSV and COVID as a combination needs to be observed closely.

Meanwhile, caution is warranted and children under the age of 5yrs need to be brought in from the storm we have left them out in. This is a group difficult to protect using "personal responsibility " and respirators. They need us to #CutDownTransmission of respiratory viruses.

Notably, past waves of RSV that have occurred, and been measured, have not been taken into account in some locations when discussing "immunity gap".

This is poor science and a huge disservice to children.

Another small but detailed study. RSV

409 infections.
83 reinfections.
Symptomatic testing only.

RSV antigenic variation plays a role.

academic.oup.com/jid/article/20…

When attempting to measure (or blame) "immunity gap", antigenic variation must be measured and accounted for. It is entirely possible that even if memory does form to RSV, it is not durable, and therefore the susceptible ( to reinfections) pool remains VAST, and is not the ->

->main contributor to the size of the wave.

Again, small but detailed study with good follow up.
75 children.
Nested cohort study.
frontiersin.org/articles/10.33…

"children infected with RSV during infancy had lower memory T cell responses at ages 2-3 years to in vitro stimulation with RSV"

"...infant RSV infection may result in greater risk of subsequent childhood respiratory viral morbidity..."

If T cell responses are impacted negatively by exposure to RSV it is entirely possible that exposure in a past wave may not be protective at all, (making immunity gap irrelevant) and opens the possibility that prior RSV and COVID exposure may be delivering a double whammy to kids

RSV and asthma.
RSV may predispose to development of asthma.
Prior exposure may have an impact on future viral illnesses, increasing likelihood of bronchospasm and need for respiratory support.

Again, does not support exposing kids to RSV to prevent future PICU admission imo.

ncbi.nlm.nih.gov/pmc/articles/P…

Further evidence supporting the potential mechanism of over active neutrophil response contributing to severe RSV and a paper showing COVID 19 results in overactive neutrophils, thereby potentially exacerbating RSV severity.

https://twitter.com/NjbBari3/status/1584549353451974661

In my view "immunity gap" is at best an unproven hypothesis, and we have many other known mechanisms of disease that can explain our observations.

I can only conclude that we must #ProtectKids from both #COVID19 and #RSV and urgently gather data on what has already happened.

@threadreaderapp please unroll.