PubMed Journals: J Infect Dis

  Source:		PMID: 32037447

    		J Infect Dis. 2020 Feb 10. pii: jiz630. doi:
     		10.1093/infdis/jiz630. [Epub ahead of print]

			Griffithsin Inhibits Nipah Virus Entry and Fusion
			and Can Protect Syrian Golden Hamsters From
			Lethal Nipah Virus Challenge.

			Lo MK(1), Spengler JR(1), Krumpe LRH(2),
			Welch SR(1), Chattopadhyay A(3), Harmon
			JR(1), Coleman-McCray JD(1), Scholte FEM(1),
			Hotard AL(1), Fuqua JL(4), Rose JK(3), Nichol
			ST(1), Palmer KE(4), O'Keefe BR(5)(6),
			Spiropoulou CF(1).

			Author Information
			(1) Viral Special Pathogens Branch, Division of
			High-Consequence Pathogens and Pathology,
			National Center for Emerging and Zoonotic
			Infectious Diseases,
			Centers for Disease Control and Prevention,
			Atlanta, Georgia, USA.
			(2) Basic Science Program, Frederick National
			Laboratory for Cancer Research, Frederick,
			Maryland, USA.
			(3) Yale University School of Medicine, New
			Haven, Connecticut, USA.
			(4) Center for Predictive Medicine for
			Biodefense and Emerging Infectious Diseases,
			University of Louisville School of Medicine,
			Louisville, Kentucky, USA.
			(5) Molecular Targets Program, Center for
			Cancer Research, National Cancer Institute,
			Frederick, Maryland, USA.
			(6) Natural Products Branch, Developmental
			Therapeutics Program, Division of Cancer
			Treatment and Diagnosis, National Cancer
			Institute, Frederick, Maryland, USA.

			Nipah virus (NiV) is a highly pathogenic zoonotic
			paramyxovirus that causes fatal encephalitis
			and respiratory disease in humans. There is
			currently no approved therapeutic for human
			use against NiV infection. Griffithsin (GRFT) is
			high-mannose oligosaccharide binding lectin
			that has shown in vivo broad-spectrum activity
			against viruses including
			severe acute respiratory syndrome coronavirus,
			human immunodeficiency virus 1, hepatitis C
			virus, and Japanese encephalitis virus. In this
			study, we evaluated the in vitro antiviral
			activities of GRFT and its synthetic trimeric
			tandemer (3mG) against NiV and other viruses
			from across 4 virus families. The 3mG had
			comparatively greater potency than GRFT
			against NiV due to its enhanced ability to block
			NiV glycoprotein-induced syncytia formation.
			Our initial in vivo prophylactic evaluation of an
			oxidation-resistant GRFT (Q-GRFT) showed
			significant protection against lethal NiV challenge
			in Syrian golden hamsters. Our results warrant
			further development of Q-GRFT and 3mG as
			potential NiV therapeutics.

			┬ęThe Author(s) 2020. Published by Oxford
			University Press for the Infectious Diseases
			Society of America. All rights reserved. For
			permissions, e-mail:

			DOI: 10.1093/infdis/jiz630 PMID: 32037447

     			                         Tweet       Print