Our latest pre-print is up!
In this study, we quantify the functional waning of non-neutralizing (effector) SARS-CoV-2 antibodies across all variants in recipients of two of the most globally administered vaccines: CoronaVac and the mRNA vaccine BNT162b2

biorxiv.org/content/10.110… We also assess how mRNA vaccine boosters in CoronaVac recipients restore & expand functional responses against variants, particularly Omicron. This is of high global health interest as CoronaVac, an inactivated vaccine, has had billions of doses administered

So what did we find?

The Sunday evening cookie chronicles I The Sunday evening cookie chronicles II

The varicella vaccination program began in 1995/6, and the incidence of chickenpox has plummeted >90%.

However, we have yet to "eliminate" varicella after 25 years of intense public health efforts and a highly effective vaccine. SARS-CoV-2, the causative agent of COVID-19, burst onto the scene in 2019. Like varicella, vaccinations were developed that are highly effective.

However, also like varicella, getting shots into arms is not easy. And reducing incidence when prevalence is high is challenging.

This succinct breakdown of the anti-public health messaging of Fox Entertainment by @chrislhayes rings all too familiar.

Throughout last year before the vaccines, I called my family members several times a week to answer any questions or concerns Most of them were great questions and I tried to help as best I could; but some questions were bonkers.

"Where did you hear that from!?" I would routinely ask, knowing damn well where they heard it from. From chloroquine to "herd immunity by infection", some were just insane

Some keep stating it's a fact that infection-acquired immunity is superior to vaccine-acquired immunity. That is simply not true.

For one not everyone survives COVID-19. Severe adverse effects from vaccines can occur, but are extremely rare. That already heavily skews the data Reports show wide variance of immune response to infection acquired immunity in survivors. Some reports show high IgG in severe COVID-19 survivors and low IgG in mild cases.
Vaccines bypass this by eliciting high IgG w/o illness
nature.com/articles/s4146…
academic.oup.com/cid/article/72…

Weird because a recent CDC MMWR came to the opposite conclusion of this "fact".

In Kentucky unvaccinated individuals were ~2.3x as likely to become re-infected with SARS-CoV-2 than those who were vaccinated.

cdc.gov/mmwr/volumes/7…

https://twitter.com/DrJBhattacharya/status/1442972888299032576

There's caveats to this study and other studies have had some other mixed results.

But to present his view as a fact shows that @DrJBhattacharya is more committed to ideology than to objective science and medicine.

There's a distinction between infection and disease state. SARS-CoV-2 is the causative agent of COVID-19. You cannot develop COVID-19 without infection with SARS-CoV-2.
COVID-19 vaccines were quantified against COVID-19, not infection. They continue to show remarkable protection. The vaccines induce an antibody response that can provide immediate protection/reduce replication of SARS-CoV-2 in the upper and lower respiratory tract. Notably, the mRNA-1273 very strongly reduces viral replication in the lower respiratory tract.
science.sciencemag.org/content/early/…

One way bad faith actors and attention seekers work is to make actual experts exhausted at correcting them. It's called "flooding the zone", and correcting the amount of mis/disinformation takes more time and energy than what experts have. (1/6) Others work to silence experts through intimidation. Not necessarily by them, but using the miscreants that follow them. This has happened to many of us in infectious diseases and public health, and continues to this day. (2/6)

Just because the initial cluster of COVID-19 cases was identified in Wuhan does NOT mean that is where the first human infection occurred. It is very possible that SARS-CoV-2 has spilled over into humans previously and was not subsequently transmitted. Viruses do this frequently Take HIV for example: HIV is the result of a spillover from simian immunodeficiency virus (SIV) that is sustained in non-human primates. There are two types of HIV: HIV-1 & HIV-2. Scientists have identified 12 lineages of them, each believed to be from an independent spillover.

The J&J vaccine reportedly confers 85% protection after 1 month. Some suggest this could be improved with a booster. About that...

J&J vaccine uses a replication-incompetent adenovirus (Ad26) to deliver the SARS-2 Spike protein. Here's what a typical adenovirus looks like: (1/5) This particular adenovirus, Ad26, was likely chosen as antibody prevalence against it is very low in humans. This allows for the presentation of the SARS-2 Spike protein without the neutralization of the vehicle (Ad26). (2/5) jvi.asm.org/content/81/9/4…

Very interesting piece by the @nytimes in regards to SARS-CoV-2 surveillance, or lack thereof, in the U.S.

Having been involved in sequencing SARS-CoV-2 among the population, I had a few thoughts.

The U.K.'s New Coronavirus Strain and How to Stop It nyti.ms/2KORogU Our group was one of the first to identify the D614G variant circulating and accumulating in North Carolina. Around the same time, other groups arrived at the same conclusion that this variant was becoming increasingly predominant.
sciencedirect.com/science/articl…

A few months ago I made the argument that working age and young adults (18-49) should be prioritized for the COVID-19 vaccine.
TL;DR I was wrong

Here's why I made the argument and why I changed by view: This is the 3rd major surge of SARS-CoV-2 in the U.S. In each surge, the data supports that the majority of transmission events were driven by young adults ==> working age ==> rest of the community. Here's Florida an example in the summer:

There's a point to be made here, but I do not think this is the way to do it.

Prevalence of SARS-CoV-2 is the primary problem. In his follow up tweet, which many may not read, Dr. Mina states that this statement doesn't apply if the test returns a positive.

https://twitter.com/michaelmina_lab/status/1334027877390688256

Keep in mind that the disease state of COVID-19 can last weeks, and in some cases, months. The worst COVID-19 complications can occur weeks post-infection, and virus footprints may only be detectable by sensitive testing such as PCR. These people need to know their health status.

Thread on miscommunication regarding SARS-CoV-2 PCR testing

False-positives by PCR testing are quite rare. It is the gold standard as it is sensitive enough to identify the virus during early and late-infection, as well as at peak viral loads. (1/6) Some may claim that PCR turnaround time renders the test useless, and I couldn't disagree more. The disease state of COVID-19 can last for a long time, and the PCR test can verify that the patient has the virus even when it's at very low levels at the tail-end of infection. (2/6)

Researchers followed-up with COVID-19 survivors weeks post-diagnosis and preformed nucleic acid and antibody diagnostics.
Results? Most patients were IgA and/or IgG positive and had less viral RNA amplified. One had actively replicating SARS-CoV-2*.

jamanetwork.com/journals/jamai… Some have floated the idea of using SARS-CoV-2 Ct as a direct quantitation of infectiousness. This is problematic because wide variability in RNA collection through NP exists. It's also impossible to tell off a single time point where the patient is in the course of infection.

A lot in this thread is, unfortunately, just not true (full disclosure I'm part of a team at UNC that validated our PCR testing).

PCR testing is by far the most sensitive way of detecting SARS-CoV-2 and the rate of false positives is actually quite low.

https://twitter.com/apoorva_nyc/status/1326728148357181443

PCR testing is being done for symptomatic patients, yes; but also for people who have been exposed to a known case, and the test can detect viral RNA before peak viral loads/symptom onset. So the claim that it's catching it too late in infection is simply false.

Not linking to his account, but a certain person using the pandemic to build his brand is tweeting more alarmist stuff.

1. Detection of viral RNA =/= infectious. To be infectious the RNA genome cannot be fragmented & virus capsid must be structurally intact. (1/4) 2. On the transmission by aerosols, the preventative methods we've emphasized for months remain largely unchanged. Wear a mask, maintain physical distancing, wash your hands, and avoid crowded areas with low/absent ventilation.
None of that has changed, nor should they. (2/4)

There's been a lot of miscommunication and misinformation about the transmissibility of SARS-CoV-2 and the severity of clinical outcomes of the disease it causes, COVID-19.

These are two very separate aspects of this virus. (1/6) COVID-19 is the disease state post-infection with SARS-CoV-2. It ranges from asymptomatic/mild symptoms to a severe set of manifestations leading to a patient being admitted into the ICU and placed on mechanical ventilation. Many of these patients may not make it out. (2/6)

My latest contribution to @smerconish is up:

Why a Fall Resurgence of COVID-19 Is Likely

smerconish.com/news/2020/9/21… A few highlights on why a resurgence is likely:

1. We have never controlled SARS-CoV-2, allowing for community spread throughout the U.S.

There's many worrying trends for SARS-CoV-2 in the U.S. right now:

1) We seem to have hit a hard floor of ~40,000 newly *confirmed cases/day. This is reminiscent of the floor we hit in May of ~20,000 per day.

*These are confirmed cases, and are underestimates (1/5) 2) Transmission increased in young adults. This happened in May when young adults saw the biggest spikes in cases.

The virus could then be transmitted as young adults tend to be more mobile. The IHME is modeling that social distancing will further relax in coming weeks (2/5)

Been seeing folks discuss the "6% only died of COVID-19 alone", and thought I'd have something productive to add since I'm an HIV virologist by training.
After years of virus spread, and in the absence of treatment, a patient infected with HIV will develop AIDS. (1/4) During this state of HIV progression, white blood cells called T-cells are depleted. This can allow co-infecting pathogens to spread unchecked or tumor cells to grow & metastasize. Hence pneumonia & AIDS-associated cancers are leading causes of death in HIV+ patients. (2/4)