This paper provides a reflexive account of conducting fieldwork as a graduate student in the Sunderban area of West Bengal state, India, in the mid-1990s. Reflecting on my personal experiences of research in a setting that was simultaneously familiar and foreign, I use frames of positionality to understand the impact of explicit and implied power structures on the research process, the relationships between the researcher and those researched, and the transfer of knowledge. This paper argues that the multiple subject positions and identities of both scholar and subjects as presented in the field vary with setting, and that these positionalities affect access to informants, the tenor and outcomes of encounters, and knowledge production. While self-reflexivity is endorsed as a strategy for critically informed research, active measures such as openness about the agenda and activities undertaken, self-disclosure, making conscious accommodations for the research subject's work schedule and time constraints, mutual sharing of information, and explicit recognition of the research subjects' expertise through lived experiences are proposed as strategies for equalising the power balance between scholar and subject.

Peripheral blood CD4+ T cell counts are a key measure for assessing disease progression and need for antiretroviral therapy in HIV-infected patients. More recently, studies have demonstrated a dramatic depletion of mucosal CD4+ T cells during acute infection that is maintained during chronic pathogenic HIV as well as SIV infection. A different clinical disease course is observed during the infection of natural hosts of SIV infection, such as sooty mangabeys (Cercocebus atys), which typically do not progress to AIDS. Previous studies have determined that SIV+ mangabeys generally maintain healthy levels of CD4+ T cells despite having viral replication comparable to HIV-infected patients. In this study, we identify the emergence of a multitropic (R5/X4/R8-using) SIV infection after 43 or 71 wk postinfection in two mangabeys that is associated with an extreme, persistent (>5.5 years), and generalized loss of CD4+ T cells (5–80 cells/μl of blood) in the absence of clinical signs of AIDS. This study demonstrates that generalized CD4+ T cell depletion from the blood and mucosal tissues is not sufficient to induce AIDS in this natural host species. Rather, AIDS pathogenesis appears to be the cumulative result of multiple aberrant immunologic parameters that include CD4+ T cell depletion, generalized immune activation, and depletion/dysfunction of non-CD4+ T cells. Therefore, these data provide a rationale for investigating multifaceted therapeutic strategies to prevent progression to AIDS, even following dramatic CD4 depletion, such that HIV+ humans can survive normal life spans analogous to what occurs naturally in SIV+ mangabeys.

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