Evidence for an Increased Risk of Transmission of Simian Immunodeficiency Virus and Malaria in a Rhesus Macaque Coinfection Model
Autor: | Ross P. Tarara, Jennifer Y. Chau, Kristina Abel, Michael G. Hudgens, JoAnn S. Sullivan, Jason P. Fine, Kristin A. Trott, Chelu K. Mfalila, William E. Collins, Shirley Luckhart |
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Rok vydání: | 2011 |
Předmět: |
Male
Plasmodium falciparum Immunology Simian Acquired Immunodeficiency Syndrome Parasitemia Biology medicine.disease_cause Microbiology Virology parasitic diseases medicine Animals Humans Viremia Transmission (medicine) Primate Diseases virus diseases Simian immunodeficiency virus medicine.disease biology.organism_classification Macaca mulatta Malaria Disease Models Animal Rhesus macaque Cerebral Malaria Insect Science Coinfection Pathogenesis and Immunity Simian Immunodeficiency Virus |
Zdroj: | Journal of Virology. 85:11655-11663 |
ISSN: | 1098-5514 0022-538X |
DOI: | 10.1128/jvi.05644-11 |
Popis: | In sub-Saharan Africa, HIV-1 infection frequently occurs in the context of other coinfecting pathogens, most importantly, Mycobacterium tuberculosis and malaria parasites. The consequences are often devastating, resulting in enhanced morbidity and mortality. Due to the large number of confounding factors influencing pathogenesis in coinfected people, we sought to develop a nonhuman primate model of simian immunodeficiency virus (SIV)-malaria coinfection. In sub-Saharan Africa, Plasmodium falciparum is the most common malaria parasite and is responsible for most malaria-induced deaths. The simian malaria parasite Plasmodium fragile can induce clinical symptoms, including cerebral malaria in rhesus macaques, that resemble those of P. falciparum infection in humans. Thus, based on the well-characterized rhesus macaque model of SIV infection, this study reports the development of a novel rhesus macaque SIV- P. fragile coinfection model to study human HIV- P. falciparum coinfection. Using this model, we show that coinfection is associated with an increased, although transient, risk of both HIV and malaria transmission. Specifically, SIV- P. fragile coinfected macaques experienced an increase in SIV viremia that was temporarily associated with an increase in potential SIV target cells and systemic immune activation during acute parasitemia. Conversely, primary parasitemia in SIV- P. fragile coinfected animals resulted in higher gametocytemia that subsequently translated into higher oocyst development in mosquitoes. To our knowledge, this is the first animal model able to recapitulate the increased transmission risk of both HIV and malaria in coinfected humans. Therefore, this model could serve as an essential tool to elucidate distinct immunological, virological, and/or parasitological parameters underlying disease exacerbation in HIV-malaria coinfected people. |
Databáze: | OpenAIRE |
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