Global Virus Network’s Institute of Human Virology and Italian Researchers identify a SARS-CoV-2 Viral Strain with Deletion in a Protein, Possibly Reducing Fatalities

A deletion in a protein, NSP1, which is important for reducing innate immune response may signal emergence of a less pathogenic viral strain Baltimore, Maryland, USA, August 24, 2020: The Institute of Human Virology (IHV) at the University of Maryland School of Medicine, a Global Virus Network (GVN) Center of Excellence, in collaboration with scientists…

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From molecular biology to human retroviruses: in memory of GVN Italy Center Director Umberto Bertazzoni (1937-2020)

Born in Trissino (VI) in 1937, Umberto Bertazzoni graduated from the University of Pavia in Pharmacy (1960) and in Biological Sciences (1964). He was a researcher at the Joint Research Center of Ispra from 1964 to 1974, researcher at the Institute of Genetics of the CNR of Pavia from 1974 to 1994 and Head of…

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Hydroxychloroquine-What’s the Deal?

The absence of efficient therapeutics for COVID-19 has brought much attention to evaluation of repurposing drugs. Hydroxychloroquine (HC) is an antimalarial drug that affects endosomal function and blocks autophagosome-lysosome fusion (1). Since coronaviruses use the endolysosomal pathway to enter the cell before uncoating, HC has been shown to inhibit SARS-CoV-2 replication in cellular models. The…

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RENOWNED DOHERTY INSTITUTE IN AUSTRALIA INDEPENDENTLY VERIFIES EARLIER FINDINGS THAT AN ANTIMICROBIAL TECHNOLOGY ERADICATES SARS-COV-2 ON SURFACES FOR MORE THAN SIX WEEKS

The Findings Corroborate Research Previously Released by the Rega Medical Research Institute of KU Leuven, Belgium Baltimore, Maryland, USA, August 13, 2020:  The Global Virus Network (GVN), a coalition comprised of the world’s preeminent human and animal virologists from 55 Centers of Excellence and 10 Affiliates in 33 countries, announced that the Peter Doherty Institute…

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The Role of Cytokine Storm in the Severity of COVID-19

There are two ways in which pathogens make us sick. One is by the direct effects of the pathogen itself. The other is by collateral damage from our hyperactive immune responses to the pathogen by the release of interferons (IFNs), interleukins (ILs), tumor-necrosis factors (TNF-α), chemokines, and several other mediators. This latter mechanism has appeared…

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