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Understanding the host response immediately following mucosal HIV-1 infection will be pivotal in determining whether the immune response induced by a vaccine will successfully sense and control viral replication. In order for effective vaccine strategies and modalities to be developed, these earliest immunological events must be fully assessed in a non-biased manner. Nonhuman primates (NHP), specifically Rhesus macaques (RM), serve as a model to investigate the immunological landscape immediately post-challenge and to define the spatiotemporal path of simian immunodeficiency virus (SIV). SIV infection of RM serves as a model of human HIV infection as it recapitulates many of the virological, immunological, and pathological features of HIV infection vii in the human host. In this thesis I will test the hypothesis whether transcriptional analysis will allow a sensitive measure of the early innate immune responses that accompany detection of the SIV virus in the periphery. I have determined that an early inflammatory profile arises early in tissues proximal to the challenge site that precedes widespread immune activation and the systemic antiviral interferon response. This study defines in detail the spatiotemporal relationship between virus and host immune response and may be a valuable resource in guiding future vaccine design strategies.
Using a Simian Immunodeficiency Virus (SIV) rhesus macaque model to study the biology of HIV-1 mucosal transmission, we demonstrated that although Toll-like receptor (TLR) agonists could induce type-1 interferon responses, it was not sufficient to prevent sexual transmission of SIV. In the animals treated with the TLR7 agonist, imiquimod, and the TLR9 agonist, CpG, we detected IFN-alpha and other anti-viral effecter molecules in vaginal-cervical secretions. However, both TLR agonists also induced proinflammatory cytokines expressions in the genital mucosa. In imiquimod treated animals, we showed a massive mononuclear cell infiltration consisting of activated CD4+ T cells, DC, and beta-chemokine-secreting cells. All the TLR agonist-treated monkeys became infected after intravaginal SIV challenge. Importantly, the set-point vRNA level in TLR ligand treated animals was significantly higher than that in control animals. We also studied the effectiveness of CpG when used as an adjuvant in combination with a therapeutic vaccine in SIV infected animals receiving antiretroviral therapy (ART). We found that compared to saline-treated control animals, the animals treated only with the therapeutic vaccine, AT2-inactivated SIV239, showed significantly lower plasma vRNA levels after ART stopped. However the CpG adjuvant treatment attenuated the protective effect of AT-2 inactivated SIV as a therapeutic AIDS vaccine, even though AT2-inactivated SIV239+CpG vaccinated animals showed augmented SIV specific IgG antibody responses as compared to all the other 3 groups. Animals treated with CpG alone showed significantly higher level of viral replication associated with increased SIV specific T cell activations. Our findings dramatically highlight the value of SIV/rhesus macaque models in studying HIV pathogenesis and evaluating the safety and efficacy of new immunological strategies to interfere with HIV infection.
A successful vaccine for the prevention and/or immunotherapy against HIV/AIDS is one of the prominent challenges of the 21st century. To date, all human vaccine trials against this virus/disease have resulted in failure, or at best have shown very low efficacy. The scientific community dealing with HIV/AIDS has unanimously proposed a focus on basic science, with the intention of identifying correlates of protection that can serve as guides in developing and evaluating vaccine preparation. However, Nature seems to have already found several ways of dealing with infections by HIV and related primate lentiviruses, either by resisting infection or, once infected, avoiding immune damage and immunodeficiency. Models of Protection Against HIV/SIV will allow for an in-depth reflection on the perspectives for vaccine and therapy research derived from important recent studies. It will be authored by some of the most well known specialists in the field of HIV resistance/protection: including F. Barré-Sinoussi (2008 Nobel Prize for Medicine winner), B. Walker, S. Rowland-Jones, A. Telenti, M. Lederman and F. Plummer. This book is structured in a unique way, looking at three models of resistance/protection separately and then comparing the models against one another to provide its readership with a detailed examination of the research that is most predominant in the search for a vaccine. This structure presents the information in an easy-to-understand format and gives the book a cross-discipline appeal -- an important reference for those in the scientific community, medical care, public health and academia alike. Provides extensive descriptions and comparisons on the different models of protection agains HIV/AIDS Comprehensive writing and illustrations Contributors are among the most eminent specialists in the field
We recently developed a novel strategy to identify transmitted HIV-1 genomes in acutely infected humans using single-genome amplification and a model of random virus evolution. Here, we used this approach to determine the molecular features of simian immunodeficiency virus (SIV) transmission in 18 experimentally infected Indian rhesus macaques. Animals were inoculated intrarectally (i.r.) or intravenously (i.v.) with stocks of SIVmac251 or SIVsmE660 that exhibited sequence diversity typical of early-chronic HIV-1 infection. 987 full-length SIV env sequences (median of 48 per animal) were determined from plasma virion RNA 1--5 wk after infection. i.r. inoculation was followed by productive infection by one or a few viruses (median 1; range 1--5) that diversified randomly with near starlike phylogeny and a Poisson distribution of mutations. Consensus viral sequences from ramp-up and peak viremia were identical to viruses found in the inocula or differed from them by only one or a few nucleotides, providing direct evidence that early plasma viral sequences coalesce to transmitted/founder viruses. i.v. infection was>2,000-fold more efficient than i.r. infection, and viruses transmitted by either route represented the full genetic spectra of the inocula. These findings identify key similarities in mucosal transmission and early diversification between SIV and HIV-1, and thus validate the SIV-macaque mucosal infection model for HIV-1 vaccine and microbicide research.
Interest in the lentivirus subfamily of retroviruses has greatly intensified due to the realization that HIV-1 and HIV-2 are members of this previously obscure group. Related lentiviruses have now been isolated from sheep, goats, horses, cattle, cats, monkeys, and humans. This issue of CTMI is devoted to the lentiviruses of nonhuman primates, referred to as simian immunodeficiency viruses (SIVs). The SIVs provide valuable tools for our quest to understand and control the HIVs, which are obviously important new human pathogens. Included in this volume are discussions of the distribution and molecular phylogeny of the SIVs and their use as animal models for the study of AIDS pathogenesis, and the chapters clearly illustrate how SIV models are contributing to our understanding of the ability of host immune responses to control infection at least temporarily and the ability of virus to evade these host immune defenses.