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Exploring the primate plasma virome:...

Bailey, Adam L.

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Exploring the primate plasma virome: Implications for human health and disease.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Exploring the primate plasma virome: Implications for human health and disease./
Author:	Bailey, Adam L.
Description:	119 p.
Notes:	Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.
Contained By:	Dissertation Abstracts International76-11B(E).
Subject:	Virology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3714358
ISBN:	9781321916119

Exploring the primate plasma virome: Implications for human health and disease.
Bailey, Adam L.

Exploring the primate plasma virome: Implications for human health and disease. - 119 p.

Source: Dissertation Abstracts International, Volume: 76-11(E), Section: B.

Thesis (Ph.D.)--The University of Wisconsin - Madison, 2015.

Wild primates serve as the immediate source and long-term reservoir of many human pathogens. However, with the exception of simian immunodeficiency viruses (SIVs), the viruses naturally harbored by these animals remain largely uncharacterized. Here, we present the discovery and characterization of several novel viruses within the Flaviviridae and Arteriviridae families referred to as GB virus C and simian arteriviruses (aka. simian hemorrhagic fever viruses), respectively. Together with SIV, it appears that these viruses are widespread and prevalent among African cercopithecoid (i.e. Old World) monkeys; thereby defining the "plasma RNA virome" of these animals. Each monkey species we examined harbors its own species-specific variant(s) of these viruses, which cause high-titer viremia in these hosts without inducing overt signs of disease. Infection studies in captive macaques and baboons infected with GBV-C and simian arteriviruses, respectively showed that these viruses are semi-persistent in these hosts but exhibit vastly different degrees of within-host genetic diversity and sequence evolution, suggesting that these viruses maintain persistence though different mechanisms. While infection of macaques with GBV-C did not elicit overt signs of disease, infection of macaques with simian arteriviruses induced high morbidity and mortality in this "non-natural" host. Given the several features of the simian arteriviruses --- vast genetic diversity, high titer and persistent infection, and the ability to transmit between primates of different species and cause disease, we believe this group of viruses merits further study and close surveillance as a zoonotic threat to human health. In contrast, our infection of macaques with baboon GBV-C created the first laboratory animal model of human GBV-C infection. With this model, we have begun to investigate the mechanism behind the widely cited but poorly understood phenomenon of GBV-C-associated protection from AIDS in HIV+ people.

ISBN: 9781321916119Subjects--Topical Terms:

642304
Virology.

Exploring the primate plasma virome: Implications for human health and disease.
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502 $a Thesis (Ph.D.)--The University of Wisconsin - Madison, 2015.
520 $a Wild primates serve as the immediate source and long-term reservoir of many human pathogens. However, with the exception of simian immunodeficiency viruses (SIVs), the viruses naturally harbored by these animals remain largely uncharacterized. Here, we present the discovery and characterization of several novel viruses within the Flaviviridae and Arteriviridae families referred to as GB virus C and simian arteriviruses (aka. simian hemorrhagic fever viruses), respectively. Together with SIV, it appears that these viruses are widespread and prevalent among African cercopithecoid (i.e. Old World) monkeys; thereby defining the "plasma RNA virome" of these animals. Each monkey species we examined harbors its own species-specific variant(s) of these viruses, which cause high-titer viremia in these hosts without inducing overt signs of disease. Infection studies in captive macaques and baboons infected with GBV-C and simian arteriviruses, respectively showed that these viruses are semi-persistent in these hosts but exhibit vastly different degrees of within-host genetic diversity and sequence evolution, suggesting that these viruses maintain persistence though different mechanisms. While infection of macaques with GBV-C did not elicit overt signs of disease, infection of macaques with simian arteriviruses induced high morbidity and mortality in this "non-natural" host. Given the several features of the simian arteriviruses --- vast genetic diversity, high titer and persistent infection, and the ability to transmit between primates of different species and cause disease, we believe this group of viruses merits further study and close surveillance as a zoonotic threat to human health. In contrast, our infection of macaques with baboon GBV-C created the first laboratory animal model of human GBV-C infection. With this model, we have begun to investigate the mechanism behind the widely cited but poorly understood phenomenon of GBV-C-associated protection from AIDS in HIV+ people.
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