Hantaviral Proteins: Structure, Functions, and Role in Hantavirus Infection

Abstract

Hantaviruses are the members of the family Bunyaviridae that are naturally maintained in the populations of small mammals, mostly rodents. Most of these viruses can easily infect humans through contact with aerosols or dust generated by contaminated animal waste products. Depending on the particular Hantavirus involved, human infection could result in either hemorrhagic fever with renal syndrome or in Hantavirus cardiopulmonary syndrome. In the past few years, clinical cases of the Hantavirus caused diseases have been on the rise. Understanding structure of the Hantavirus genome and the functions of the key viral proteins are critical for the therapeutic agents’ research. This paper gives a brief overview of the current knowledge on the structure and properties of the Hantavirus nucleoprotein and the glycoproteins.

RIG-I-like receptor activation drives type I IFN and antiviral signaling to limit Hantaan orthohantavirus replication

“…HTNV is a member of the family Hantaviridae, tri-segmented, negative-sense, singlestranded RNA viruses in the order Bunyavirales. The three genome segments, referred to as small (S), medium (M), and large (L), encode four viral proteins; the viral nucleocapsid (N), the two viral surface glycoproteins (Gc and Gn), and the RNA-dependent RNA polymerase (L) [1,7]. Around the world, hantaviruses have been identified in diverse reservoir hosts, but human pathogenic hantaviruses are, as yet, only found in rodent reservoir hosts [8,9].…”

Hantavirus Infections in the European Region: A Mini-Review of the Literature

“…Viral cell entry is mediated through Hantavirus surface glycoproteins after interaction with host cell membrane proteins [3]. Specifically, infective virions attach and enter vascular endothelial cells after interacting with cell surface αvβ3-integrins [11]. The pathogenetic mechanism of the underlying vascular permeability increase, during a Hantavirus infection, is common between HFRS and HPS.…”

TRAF3 signaling: Competitive binding and evolvability of adaptive viral molecular mimicry

“…Gn protein (also known as G1) of NY-1 Hantavirus [68,69] and M protein of SARS Coronavirus [67] also disrupts the formation of TRAF3-TBK1 complex and inhibits IFN production. Structures of these proteins are not available.…”