Top 10 most downloaded articles in 2020 includes our review in the @AnnualReviews Virology - “Seasonality of Respiratory Viral Infections” by @MiyuMoriyama et al! It’s free to download: arevie.ws/3aYt32Y
Here let’s highlight other relevant pieces on the same topic (1/n)
Just to recap, seasonal factors that drive respiratory tract viral infections are mainly these three;
1) ⬇️ Temperature 2) ⬇️ Humidity (esp. indoor) 3) ⬇️ Sunlight/Vitamin D
(2/n)
A twitter thread that demonstrates the importance of humidity on antiviral defense through mucociliary clearance measured by @Ericsongg. (3/n)
An elegant in vivo study demonstrating evidence for vitamin D3 supplementation in enhancing antiviral immunity in older adults by @Emma_S_Chambers & colleagues. (7/n)
A computer simulation comparing viral spread at 10% vs. 60% relative humidity. 後半に日本語のコメンタリーあり。Love the bgm 🎶 (8/n).
I also recommend this very cool hypothesis piece by @anice_lowen and Peter Palese on the “Transmission of influenza virus in temperate zones is predominantly by aerosol, in the tropics by contact” (9/n)
In my lab, it all began with a study by the awesome @ellenfoxman in which she showed that cooler temperature dampens innate antiviral immune defense. pnas.org/content/112/3/…
Now I have to go get dinner ready. If anyone wants to add more resources to this thread on how seasonal factors influence respiratory viral infections, that would be great! Thank you 🙏🏼 (end)
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What is the relevance of viral load in #COVID19 disease severity? A very talented @YaleMSTP student @SilvaJ_C found that saliva viral load to be a better predictor of disease than nasopharyngeal viral load. Here is a thread to explain the findings. (1/n)
I preface by saying that numerous fantastic studies by many have demonstrated nasopharyngeal viral load to correlate with disease severity and mortality, while others do not find such correlation. Here are some of these studies. (2/n)
Being at @yale, the birthplace of #SalivaDirect and everything saliva bc of awesome colleagues like @awyllie13@NathanGrubaugh@VogelsChantal et al, we had access to both saliva and nasopharyngeal (NP) samples from the same patients to do direct comparisons. (3/n)
My first tweet of 2021 is going to be about 1 dose vs. 2 dose vaccine. I have tweeted in the past of the immunological advantages of a 2 dose vaccine. However, given the enhanced transmission variants on the rise, we need a modified strategy. (1/n)
We typically give vaccines in more than one dose to increase 1) quantity, 2) quality, 3) longevity of antibody responses. This holds true for most vaccines including mRNA vaccines. Here is what I tweeted about this before. (2/n)
However, the 2 dose vaccine with limited number of vaccine means only half the people getting vaccinated at this time. If the virus is spreading slowly, we want to do the right thing and give the most vulnerable 2 doses and others to wait. (3/n)
Inspired by this tweet by @TheMenacheryLab, I reached out to the wonderful colleagues at the @serimmune to see if the other mutations found in the B.1.1.7 variant would evade antibody responses generated by the wild type #SARSCOV2. (1/n)
According to this report, B.1.1.7 harbors non-synonymous mutations in the following viral genes, resulting in truncation, deletions and amino acid changes. Would these mutations result in evasion from antibodies generated by wild type virus? (2/n)
To probe this possibility, @serimmune used their technology platform based on bacterial display peptide libraries, next generation sequencing & machine learning to reveal antibody reactivity against WT and B.1.1.7 viral antigens. (3/n)
What aspects of antibody responses determine the outcome of #COVID19? In this new preprint by @carolilucas@sneakyvirus1 et al., we found that the early timing of antibody response (before 14 days of symptom) in infected person is key to recovery. (1/n)
However, patients with lethal COVID did not have the highest level of anti-S or anti-RBD antibodies. What’s going on? (2/n)
To understand better the features of antibody responses in patients who died vs. survived, we compared their time course. We found a delay in antibody responses in lethal disease. We also noted patients with very high neutralizing Ab (HN) with very early antiviral Abs. (3/n)
How do we look for autoantibodies against a wide range of self antigens? The @aaronmring lab developed a high-throughput autoantibody discovery technique called Rapid Extracellular Antigen Profiling (REAP) against 2,770 extracellular and secreted proteins "exoproteome" 💪🏼 (2/n)
A large fraction of #COVID patients had autoantibodies to multiple self antigens. The more severe the disease, more autoantibodies they had.(3/n)
Here is a thread to explain the findings of this study, that used computational tools to predict T cell reactive sequences in #SARSCOV2 subunit vaccines.
Our adaptive immune system has 2 types of white blood cells known as lymphocytes. T cells and B cells. These lymphocytes give us protection from wide variety of pathogens. Each lymphocyte has unique receptor that detect specific features of a pathogen. (2/n)
B cells detect pathogens structures through antibodies. T cells cannot detect pathogens on their own. They can only “see” pathogen when tiny pieces of viral proteins (peptides) are presented by molecules called major histocompatibility complex (MHC). (3/n)