SARS-CoV-2 Load does not Predict Transmissibility in College Students

SARS-CoV2 is highly contagious and the global spread has caused significant medical, social and economic impacts. Other than vaccination, effective public health measures, including contact tracing, isolation and quarantine, is critical for deterring viral transmission, preventing infection progression and resuming normal activities. Viral transmission is affected by many factors but the viral load and vitality could be among the most important ones. Although in vitro culture studies have indicated that the amount of virus isolated from infected people determines the successful rate of virus isolation, whether the viral load carried at the individual level would affect the transmissibility was not known. We aimed to determine whether the Ct value, a measurement of viral load by RT-PCR assay, could differentiate the spreader from the non-spreader in a population of college students. Our results indicate that while at the population level the Ct value is lower, suggesting a higher viral load, in the symptomatic spreaders than the asymptomatic non-spreaders, there is a significant overlap in the Ct values between the two groups. Thus Ct values, or the viral load, at the individual level could not predict the transmissibility. Our studies also suggest that a sensitive method to detect the presence of virus is needed to identify asymptomatic persons who may carry a low viral load but can still be infectious.

Extracellular vesicle activities regulating macrophage- and tissue-mediated injury and repair responses

Macrophages are typically identified as classically activated (M1) macrophages and alternatively activated (M2) macrophages, which respectively exhibit pro- and anti-inflammatory phenotypes, and the balance between these two subtypes plays a critical role in the regulation of tissue inflammation, injury, and repair processes. Recent studies indicate that tissue cells and macrophages interact

The Integrin Binding Peptide, ATN-161, as a Novel Therapy for SARS-CoV-2 Infection

Many efforts to design and screen therapeutics for severe acute respiratory syndrome coronavirus (SARS-CoV-2) have focused on inhibiting viral cell entry by disrupting ACE2 binding with the SARS-CoV-2 spike protein. This work focuses on inhibiting SARS-CoV-2 entry through a hypothesized 5{beta}1 integrin-based mechanism, and indicates that inhibiting the spike protein interaction with 5{beta}1 integrin (+/- ACE2), and the interaction between 5{beta}1 integrin and ACE2 using a molecule ATN-161 represents a promising approach to treat COVID-19.