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More rapid, robust and sustainable antibody responses to mRNA COVID-19 vaccine in convalescent COVID-19 individuals

Congratulations to the dozens of WCM Pathology members who co-authored or volunteered for the new study, "More rapid, robust and sustainable antibody responses to mRNA COVID-19 vaccine in convalescent COVID-19 individuals," in The Journal of Clinical Invesitgation. 


Longitudinal studies are needed to evaluate the SARS-CoV-2 mRNA vaccine antibody response under “real-world” conditions. This longitudinal study investigated the quantity and quality of SARS-CoV-2 antibody response in 846 specimens from 350 subjects: comparing BNT162b2-vaccinated individuals (19 previously diagnosed with COVID-19 [RecoVax]; 49 never been diagnosed [NaïveVax]) to 122 hospitalized unvaccinated (HospNoVax) and 160 outpatient unvaccinated (OutPtNoVax) COVID-19 patients.

NaïveVax experienced a delay in generating SARS-CoV-2 total antibody levels (TAb) and neutralizing antibodies (SNAb) after the 1st vaccine dose (D1), but a rapid increase in antibody levels was observed after the 2nd dose (D2). However, these never reached the robust levels observed in RecoVax. In fact, NaïveVax TAb and SNAb levels decreased 4-weeks post-D2 (p=0.003;p<0.001). For the most part, RecoVax TAb persisted throughout this study, after reaching maximal levels 2-weeks post-D2; but SNAb decreased significantly ~6-months post-D1 (p=0.002). Although NaïveVax avidity lagged behind that of RecoVax for most of the follow-up periods, NaïveVax did reach similar avidity by ~6-months post-D1. These data suggest that one vaccine dose elicits maximal antibody response in RecoVax and may be sufficient. Also, despite decreasing levels in TAb and SNAb overtime, long-term avidity maybe a measure worth evaluating and possibly correlating to vaccine efficacy.

Read the full article here

Serendipity opens new path toward osteoporosis treatment

A cellular protein whose normal function appears to suppress bone formation may be a potential new target for treating osteoporosis, according to a collaborative study led by Weill Cornell Medicine and NewYork-Presbyterian investigators.

Matthew Greenblatt, MD, PhD
Associate Professor of Pathology and Laboratory Medicine

In the study, published July 29 in Nature Communications, researchers discovered that mice lacking the cellular protein SLITRK5, found on the surface of bone-forming osteoblast cells, built more bone tissue than their SLITRK5-expressing kin. Laboratory experiments from the mice confirmed that the difference is principally due to the cellular protein’s absence.

Cells expressing the protein SLITRK5 are marked with magenta (left) and a marker of bone-forming osteoblasts in green (middle). These markers were viewed in the spongy bone in the marrow space (top) or on the outer layer covering the bone (bottom). Overlap between these two markers (right) shows that SLITRK5 is in bone-forming osteoblasts but not other cell types, helping make SLITRK5 a target for the treatment of skeletal diseases.

“This cell surface protein is a new negative regulator of bone formation,” said senior author Dr. Matthew Greenblatt, an associate professor of pathology and laboratory medicine at Weill Cornell Medicine and a pathologist at NewYork-Presbyterian/Weill Cornell Medical Center. “Those are really the most valuable genes for us to discover, because when we inhibit them with an antibody or by other methods, they could augment bone formation and be potential therapeutic targets for osteoporosis and related disorders.”

Osteoporosis, a systemic condition in which bones are prone to fractures due to insufficient density, is the most common bone disease, afflicting about 10 million people in the United States alone. The disease is especially common in women, with nearly 20% of women over age 50 having osteoporosis, and over half exhibiting the precursor condition of low bone mass.

Dr. Paul D. Simonson Selected for 2021 Lab/Translational AMC Scholar Award Program

Paul D. Simonson, MD, PhD
Assistant Professor of Clinical Pathology and Laboratory Medicine

The AIDS Malignancy Consortium (AMC) Executive Committee selected our colleague Dr. Paul D. Simonson to participate in its prestigious 2021 Lab/Translational Scholar Award Program!

The Scholar Award Program was established to encourage and foster the development of new and junior clinical investigators at AMC domestic and international sites to pursue careers in clinical research trials in HIV associated malignancies within the context of the AMC.

Congratulations Dr. Simonson!

Weill Cornell Medicine Pathology & Laboratory Medicine 1300 York Avenue New York, NY 10065 Phone: (212) 746-6464 Fax: (212) 746-8192