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Abstract
Chronic immune activation and progression to AIDS are observed after SIV infection in macaques but not in natural host primate species. To better understand this dichotomy, we compared acute pathogenic SIV infection in pigtailed macaques (PTs) to non-pathogenic infection in African green monkeys (AGMs). SIVagm-infected PTs, but not SIVagm-infected AGMs, rapidly developed systemic immune activation, marked and selective depletion of IL-17-secreting (Th17) cells, and loss of the balance between Th17 and T regulatory (Treg) cells in blood, lymphoid organs, and mucosal tissue. The loss of Th17 cells was found to be predictive of systemic and sustained T cell activation. Collectively, these data indicate that loss of the Th17 to Treg balance is related to SIV disease progression.
Highlights
Progressive disease caused by the human immunodeficiency virus, type 1 (HIV) is marked by systemic inflammation and immune dysregulation, most notably CD4+ T cell depletion [1,2,3,4]
In the pigtailed macaques (PTs), viremia was associated with CD4+ T cell depletion in the peripheral blood and multiple signs of persistent immune activation and inflammation
The primary isolate SIVagm.Sab92018 was used to infect (IV, 600 TCID50) four pigtailed macaques (PT; Macaca nemestrina) and four African green monkeys (AGM; Chlorocebus sabaeus). This primary isolate is derived from a wild-caught chronically SIVinfected C. sabaeus AGM from Senegal [25] and causes acquired immunodeficiency syndrome (AIDS) in 50% of infected pigtailed macaques within two years
Summary
Progressive disease caused by the human immunodeficiency virus, type 1 (HIV) is marked by systemic inflammation and immune dysregulation, most notably CD4+ T cell depletion [1,2,3,4]. SIV infection of the African green monkey (AGM) results in high viral loads in blood and lymphoid tissues, but limited inflammation and chronic immune activation, and no pathology [6,9,10,11,12] It is not clear why some lentiviral infections trigger high levels of inflammation while others do not, it is evident that decisive host-pathogen interactions take place early after infection and can be determinants of disease progression. The mechanisms by which this ‘‘immune activation set point’’ is established after acute infection have been difficult to elucidate It is known, for example, that pathogenic SIV and HIV infections lead to rapid depletion of CD4+ T cells in the lamina propria of the gut, with impaired integrity of the mucosal epithelium, enhanced bacterial translocation, and perhaps systemic immune activation [16,17]. Acute CD4+ T cell depletion in the gut occurs in the setting of ‘‘nonpathogenic’’ SIV infection [18,19], raising the question as to when and how differential host responses to lentiviral infection are established
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