Cellular immune responses in rhesus macaques infected rectally with low dose simian immunodeficiency virus

Ms, Salvato; Emau, Peter; Malkovsky, Miroslav; Kt, Schultz; Johnson, Erik E.; Cd, Pauza

doi:10.1111/j.1600-0684.1994.tb00112.x

Cited by 38 publications

(15 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the SIV model shows that low doses of pathogenic virus can lead to a latent infection in monkeys. In such animals, virus replication seems to be suppressed early after infection by a virus-specific cellular immune response (Dittmer et al, 1995 b, c ;Salvato et al, 1994). This observation is supported by reports on specific T cell responses in HIV-seronegative individuals exposed to HIV (Shearer & Clerici, 1996).…”

Section: Infection Of Macaques With Immunodeficiency Virusessupporting

confidence: 74%

“…It has been reported that SIV-specific Th induced by low doses of infectious SIV might confer protection against a highdose challenge (Salvato et al, 1994 ;Clerici et al, 1994). This is in line with the hypothesis that humans exposed to low doses or defective strains of HIV develop virus-specific Th and are subsequently resistant to the consequences of HIV superinfection (Clerici & Shearer, 1993).…”

Section: Conclusion Implications For Vaccination and Therapy Againstmentioning

confidence: 99%

See 1 more Smart Citation

Long-term non-progressive human immunodeficiency virus infection: new insights from the simian immunodeficiency virus model.

Dittmer

Hunsmann²

1997

Journal of General Virology

View full text Add to dashboard Cite

Section: Infection Of Macaques With Immunodeficiency Virusessupporting

confidence: 74%

Section: Conclusion Implications For Vaccination and Therapy Againstmentioning

confidence: 99%

Long-term non-progressive human immunodeficiency virus infection: new insights from the simian immunodeficiency virus model.

Dittmer

Hunsmann²

1997

Journal of General Virology

View full text Add to dashboard Cite

“…Ag dose is also known to affect the Th1/Th2 phenotype of the ensuing response. Most in vivo observations show that lower and higher doses, respectively, favor the generation of Th1 and Th2 cells (5,(25)(26)(27)(28)(29)(30), although some in vitro observations are inconsistent with this conclusion (31).…”

mentioning

confidence: 72%

The Number of Responding CD4 T Cells and the Dose of Antigen Conjointly Determine the Th1/Th2 Phenotype by Modulating B7/CD28 Interactions

Rudulier

McKinstry

Al‐Yassin

et al. 2014

The Journal of Immunology

View full text Add to dashboard Cite

Our previous in vivo studies show that both the amount of Ag and the number of available naive CD4 T cells affect the Th1/Th2 phenotype of the effector CD4 T cells generated. We examined how the number of OVA-specific CD4 TCR transgenic T cells affects the Th1/Th2 phenotype of anti-SRBC CD4 T cells generated in vivo upon immunization with different amounts of OVA-SRBC. Our observations show that a greater number of Ag-dependent CD4 T cell interactions are required to generate Th2 than Th1 cells. We established an in vitro system that recapitulates our main in vivo findings to more readily analyze the underlying mechanism. The in vitro generation of Th2 cells depends, as in vivo, upon both the number of responding CD4 T cells and the amount of Ag. We demonstrate, using agonostic/antagonistic Abs to various costimulatory molecules or their receptors, that the greater number of CD4 T cell interactions, required to generate Th2 over Th1 cells, does not involve CD40, OX40, or ICOS costimulation, but does involve B7/CD28 interactions. A comparison of the level of expression of B7 molecules by APC and CD4 T cells, under different conditions resulting in the substantial generation of Th1 and Th2 cells, leads us to propose that the critical CD28/B7 interactions, required to generate Th2 cells, may directly occur between CD4 T cells engaged with the same B cell acting as an APC.

show abstract

“…Studies of the simian AIDS models have also suggested that cell-mediated immune responses play an important role in protection against simian immunodeficiency virus infection (34). It is possible that some genetic factors including HLA haplotype may also contribute to the development of resistance to HIV-1 infection (1, 8, 9).…”

Section: Discussionmentioning

confidence: 99%

Protective immunity to HIV-1 in SCID/beige mice reconstituted with peripheral blood lymphocytes of exposed but uninfected individuals

Zhang

Cui

Houston

et al. 1996

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

View full text Add to dashboard Cite

Immunodeficiency typically appears many years after initial HIV infection. This long, essentially asymptomatic period contributes to the transmission of HIV in human populations. In rare instances, clearance of HIV-1 infection has been observed, particularly in infants. There are also reports of individuals who have been frequently exposed to HIV-1 but remain seronegative for the virus, and it has been hypothesized that these individuals are resistant to infection by HIV-1. However, little is known about the mechanism of immune clearance or protection against HIV-1 in these highrisk individuals because it is difficult to directly demonstrate in vivo protective immunity. Although most of these high-risk individuals show an HIV-1-specific cell-mediated immune response using in vitro assays, their peripheral blood lymphocytes (PBLs) are still susceptible to HIV infection in tissue culture. To study this further in vivo, we have established a humanized SCID mouse infection model whereby T-, B-, and natural killer-cell defective SCID͞beige mice that have been reconstituted with normal human PBLs can be infected with HIV-1. When the SCID͞beige mice were reconstituted with PBLs from two different multiply exposed HIV-1 seronegative individuals, the mice showed resistance to infection by two strains of HIV-1 (macrophage tropic and T cell tropic), although the same PBLs were easily infected in vitro. Mice reconstituted with PBLs from non-HIV-exposed controls were readily infected. When the same reconstituted mice were depleted of human CD8 T cells, however, they became susceptible to HIV-1 infection, indicating that the in vivo protection required CD8 T cells. This provides clear experimental evidence that some multiply exposed, HIV-1-negative individuals have in vivo protective immunity that is CD8 T celldependent. Understanding the mechanism of such protective immunity is critical to the design and testing of effective prophylactic vaccines and immunotherapeutic regimens.

show abstract

Cellular immune responses in rhesus macaques infected rectally with low dose simian immunodeficiency virus

Cited by 38 publications

References 25 publications

Long-term non-progressive human immunodeficiency virus infection: new insights from the simian immunodeficiency virus model.

Long-term non-progressive human immunodeficiency virus infection: new insights from the simian immunodeficiency virus model.

The Number of Responding CD4 T Cells and the Dose of Antigen Conjointly Determine the Th1/Th2 Phenotype by Modulating B7/CD28 Interactions

Protective immunity to HIV-1 in SCID/beige mice reconstituted with peripheral blood lymphocytes of exposed but uninfected individuals

Contact Info

Product

Resources

About