Suppression of Human Immunodeficiency Virus Replication during Acute Measles

Tamura

The American Journal of Tropical Medicine and Hygiene

2003

Abstract. While a number of microbial infections induce a transient burst in viral load in individuals infected with human immunodeficiency virus-1 (HIV-1), a recent study has suggested that scrub typhus may suppress HIV-1 infection. We investigated the effects of Orientia tsutsugamushi on HIV-1 infection. In vitro HIV-1 infection experiments were conducted using peripheral blood mononuclear cells (PBMC) acutely infected with R5 and X4 HIV-1 or PBMC derived from patients receiving highly active antiretroviral therapy (HAART) whose plasma viral load was undetectable. Stimulation of PBMC with O. tsutsugamushi induced production of proinflammatory cytokines and ␤-chemokines, and markedly down-regulated expression of CCR5. Although pretreatment with O. tsutsugamushi rendered PBMC resistant to R5 HIV-1, it otherwise enhanced HIV-1 replication. Stimulation by O. tsutsugamushi induced HIV-1 replication in PBMC from patients receiving HAART. These findings suggest that scrub typhus does not necessarily suppress HIV-1 infection and does have potential to enhance HIV-1 replication.

Section: Discussionsupporting

confidence: 51%

In Vitro Reactivation of Human Immunodeficiency Virus-1 Upon Stimulation With Scrub Typhus Rickettsial Infection

Tamura

The American Journal of Tropical Medicine and Hygiene

2003

Proc. Natl. Acad. Sci. U.S.A.

“…HIV-positive people with acute dengue or measles viruses infection have marked reductions in plasma HIV RNA concentration, suggesting viral interference (44,45). Although measles viruses has been shown to inhibit HIV replication independent of chemokines in vitro (46), several members of the Flavivirus family (HCV, Japanese Encephalitis Virus and Dengue Virus) alter the cellular release of cytokines and chemokines (47)(48)(49).…”

Section: Discussionmentioning

confidence: 99%

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 ⁺ Jurkat T cells

Xiang

McLinden

Chang

et al. 2006

115

“…Some persons who are simultaneously infected with HIV-1 and either dengue, Orienta tsutsugamushi, hepatitis G/GB virus C, or measles morbilli virus have reduced viral loads compared with patients who are infected with HIV-1 alone or with HIV-1 and other pathogens. [17][18][19][20][21][22][23][24][25] In the case of hepatitis G virus (HGV), the mechanism of action is postulated to be via binding of the serum HGV E2 protein to CD81, leading to increased regulated on activation normal T expressed and secreted protein (RANTES) secretion and reduced CCR5 expression. 24 In vitro studies have shown that HTLV-type 2 infection might up-regulate the production of macrophage inflammatory protein-1␣ (MIP-1␣).…”

Section: Introductionmentioning

confidence: 99%

Noninfectious papilloma virus–like particles inhibit HIV-1 replication: implications for immune control of HIV-1 infection by IL-27

Fakruddin

Lempicki

Gorelick

et al. 2006

Blood

122

Human papilloma virus (HPV)- IntroductionIt has been demonstrated that both innate and adaptive immune response regulate HIV-1 replication, 1-10 and certain cell types secrete soluble HIV-1-suppressing proteins in response to various stimuli. [11][12][13][14][15] For example, secretion of anti-HIV ␤-chemokines and CD8 antiviral factor (CAF) from human T-lymphotropic virus (HTLV)-type 1 and herpes virus saimiri-infected cell line have been described. [11][12][13][14][15] Although a combination of antibodies and suppressive factors was able to reverse the inhibitory activity of CAF, complete reversal of HIV-1 suppression was not observed, suggesting that additional unknown suppressive factors were involved. 16 Certain microbial organisms elicit immune responses that reduce clinical HIV-1 infection presumably through the induction of soluble suppressive factors. Some persons who are simultaneously infected with HIV-1 and either dengue, Orienta tsutsugamushi, hepatitis G/GB virus C, or measles morbilli virus have reduced viral loads compared with patients who are infected with HIV-1 alone or with HIV-1 and other pathogens. [17][18][19][20][21][22][23][24][25] In the case of hepatitis G virus (HGV), the mechanism of action is postulated to be via binding of the serum HGV E2 protein to CD81, leading to increased regulated on activation normal T expressed and secreted protein (RANTES) secretion and reduced CCR5 expression. 24 In vitro studies have shown that HTLV-type 2 infection might up-regulate the production of macrophage inflammatory protein-1␣ . 26 Recent studies demonstrate that human papillopma virus-like particles (HPV-VLPs) bind to dendritic cells and are able to induce a range of responses in immune cells, notably the expression of anti-HIV-1 cytokines such as interferon-␣ (IFN-␣), interleukin-10 (IL-10), interferon-␥ (IFN-␥), and monocyte chemotactic protein 2 (MCP-2). 27,28 The HPV-VLP vaccine has been demonstrated to be protective against HPV infection. 29-31 HPV-type 16 (HPV16) represents the primary causative agent of cervical cancer. 32 The HPV16 VLPs, composed of the L1 major capsid protein, form nonenveloped icosahedral particles that lack viral DNA but both morphologically and immunologically resemble native virions. 33 Studies suggest that a potent immune response induced by VLPs is through the Toll-like receptor (TLR)/MyD88 pathway in dendritic cells. 27 In the current work, we evaluated the impact of VLPs on HIV-1 replication. Our results demonstrated that VLPs strongly inhibit replication of X4 and R5 HIV-1 in peripheral blood mononuclear cells (PBMCs) and monocyte-derived macrophages (MDMs). It was discovered that the anti-HIV-1 activity of VLPs involved the release of suppressive factors. Gene expression profiles of PBMCs and MDMs demonstrated that VLP treatment up-regulated numerous potential antiviral genes along with the induction of recently described cytokine . Subsequent experiments demonstrated that recombinant IL-27 was able to inhibit X4 and R5 HIV replication. Taken together, these s...