Genetic mapping of the Mx influenza virus resistance gene within the region of mouse chromosome 16 that is homologous to human chromosome 21

Reeves, Roger H.; O’Hara, Bruce F.; Pavan, William J.; Gearhart, John D.; Haller, Otto

doi:10.1128/jvi.62.11.4372-4375.1988

Cited by 48 publications

(6 citation statements)

References 21 publications

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“…Mx1-bearing mice survive infection with mouse-adapted IAV at doses that are lethal for standard inbred strains. The Mx1 gene is located on chromosome 16 in a region that is syntenic with the long arm of human chromosome 21 (Reeves et al 1988). Mx1 is functional in wild mouse species (Haller et al 1987) and wild mouse-derived strains (Ferris et al 2013;Jin et al 1998;Maurizio et al 2018;Nurnberger et al 2016;Vanlaere et al 2008) and may protect wild mice from infection with influenza-like viruses transmitted by ticks and possibly other pathogens.…”

Section: From Mx1-positive Mice To Human Mx1mentioning

confidence: 99%

Mx genes: host determinants controlling influenza virus infection and trans-species transmission

Haller

Kochs

2019

Hum Genet

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The human MxA protein, encoded by the interferon-inducible MX1 gene, is an intracellular influenza A virus (IAV) restriction factor. It can protect transgenic mice from severe IAV-induced disease, indicating a key role of human MxA for host survival and suggesting that natural variations in MX1 may account for inter-individual differences in disease severity among humans. MxA also provides a robust barrier against zoonotic transmissions of avian and swine IAV strains. Therefore, zoonotic IAV must acquire MxA escape mutations to achieve sustained human-to-human transmission. Here, we discuss recent progress in the field.

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Section: From Mx1-positive Mice To Human Mx1mentioning

confidence: 99%

Mx genes: host determinants controlling influenza virus infection and trans-species transmission

Haller

Kochs

2019

Hum Genet

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“…However, the allele(s) underlying any possible human susceptibility to avian influenza infection remain(s) unknown (reviewed in [30-31, 46]). One possibility is the MxA protein, which is the human homolog of mouse Mx1 and is encoded on chromosome 21 [47]. Although the MxA protein has been shown to be an antiviral factor [24,48], the mechanism underlying allelic phenotypic variation within the MxA gene and a connection to human susceptibility to IAV infection and pathogenicity remains an evolving area of investigation.…”

Section: Human Genetic Determinants That Modulate Iav Infectionmentioning

confidence: 99%

Host genetic determinants of influenza pathogenicity

Lin

Brass

2013

Current Opinion in Virology

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Despite effective vaccines, influenza remains a major global health threat due to the morbidity and mortality caused by seasonal epidemics, as well as the 2009 pandemic. Also of profound concern are the rare but potentially catastrophic transmissions of avian influenza to humans, highlighted by a recent H7N9 influenza outbreak. Murine and human studies reveal that the clinical course of influenza is the result of a combination of both host and viral genetic determinants. While viral pathogenicity has long been the subject of intensive efforts, research to elucidate host genetic determinants, particularly human, is now in the ascendant, and the goal of this review is to highlight these recent insights.

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“…It was observed in the 1960s that wild mice were resistant to influenza viruses, whereas most inbred mice were susceptible (Lindenmann, 1962). This trait was later mapped to a locus on mouse chromosome 16 (Haller et al, 1987;Reeves et al, 1988;1986b). The underlying gene products (named Mx) were first detected in a two-dimensional electrophoresis of lysates from Mx +/+ and Mx À/À mouse cells that were treated with type I interferon (Horisberger et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

The Interferon-Inducible MxB Protein Inhibits HIV-1 Infection

Liu

Pan

Ding

et al. 2013

Cell Host & Microbe

308

390

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The interferon-inducible myxovirus resistance (Mx) proteins play important roles in combating a wide range of virus infections. MxA inhibits many RNA and DNA viruses, whereas the antiviral activity of MxB is less well established. We find that human MxB inhibits HIV-1 infection by reducing the level of integrated viral DNA. Passaging HIV-1 through MxB-expressing cells allowed the evolution of a mutant virus that escapes MxB restriction. HIV-1 escapes MxB restriction by mutating the alanine residue at position 88 in the viral capsid protein (CA), with a consequent loss of CA interaction with the host peptidylprolyl isomerase cyclophilin A (CypA), suggesting a role for CypA in MxB restriction. Consistent with this, MxB associates with CypA, and shRNA-mediated CypA depletion or cyclosporine A treatment resulted in the loss of MxB inhibition of HIV-1. Taken together, we conclude that human MxB protein inhibits HIV-1 DNA integration by a CypA-dependent mechanism.

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Genetic mapping of the Mx influenza virus resistance gene within the region of mouse chromosome 16 that is homologous to human chromosome 21

Cited by 48 publications

References 21 publications

Mx genes: host determinants controlling influenza virus infection and trans-species transmission

Mx genes: host determinants controlling influenza virus infection and trans-species transmission

Host genetic determinants of influenza pathogenicity

The Interferon-Inducible MxB Protein Inhibits HIV-1 Infection

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