Lack of evidence of viability and infectivity of SARS-CoV-2 in the fecal specimens of COVID-19 patients.

SARS-CoV-2 can be shed in feces and can enter sewage systems. In order to implement effective control measures and identify new channels of transmission, it is essential to identify the presence of infectious virus particles in feces and sewage. In this study, we attempt to utilize Molecular techniques, cell cultures and animal models to find out the infectivity of SARS-CoV-2 in the feces of COVID-19 patients. Our findings exclude the presence of infectious virus particles, suggesting that fecal-oral transmission may not be the main mode of transmission. Larger-scale initiatives are nevertheless required, particularly considering the emergence of new viral strains.

Dengue Virus NS1 Exposure Affects von Willebrand Factor Profile and Platelet Adhesion Properties of Cultured Vascular Endothelial Cells.

Hematological abnormalities and altered vascular permeability are frequently encountered in Dengue virus infected patients, but the mechanisms that alter platelet-endothelium interactions remain incompletely understood. The DENV NS1 protein has been implicated in adverse disease outcomes. In the present study the role of NS1 protein in affecting the expression of vWF and platelet adhesion properties of endothelial cells was studied in vitro. The results suggest that vWF is down regulated in cultured endothelial cells 6 and 24 h after exposure with increase in vWF levels in culture supernatants at corresponding time points. Ultrastructural studies showed distinct evidence of endothelial cell activation morphology and degranulation of Weibel-Palade bodies in NS1 exposed cells that also showed increased platelet activation physiology. The findings suggest that changes in vWF production and secretion may be induced in endothelial cells exposed to DENV NS1 protein; and play a role in bleeding complications of severe DENV disease.

An Early Passage Human Isolate of Kyasanur Forest Disease Virus Shows Acute Neuropathology in Experimentally Infected CD-1 Mice.

BACKGROUND: Kyasanur Forest disease virus (KFDV) is a tick-borne Flavivirus that causes a severe illness in humans. Disease spectrum can vary from subclinical infection to fatal cases with hemorrhagic complications. The pathology of KFDV remains incompletely understood. METHODS: This study describes the histopathologic and immunohistochemical findings in experimentally infected infant CD-1 mice with an early passage human KFDV isolate. RESULTS: Acute histological changes were primarily seen in the brain. The spectrum of changes included gliosis, inflammatory response, necrosis, neural loss, and syncytium formation in mid and hind brain structures. Microscopic lesions observed in the liver were mainly necrosis and vacuolation of hepatocytes and in small intestine, prominent epithelial cell necrosis. KFDV antigens could be stained by a sensitive immunohistochemical labeling in the same organs. CONCLUSIONS: Findings from this study are suggestive of neuropathology as the main manifestation of an early passaged human KFDV isolate. Importantly, this suggests that KFDV may be causing primarily a neurologic disease and secondary organ damage could be because of disease pathology per se. The use of primary low passage human isolates and neuropathology profile could also be more apt in developing a challenge model for testing potential antivirals and therapeutic agents.