Abstract

Human Immunodeficiency Virus (HIV) infection presents a multifaceted challenge, extending
beyond its primary impact on the immune system to affect various organ systems. Among
these, the bone marrow, the primary site for hematopoiesis, undergoes substantial
alterations during HIV infection, profoundly influencing erythropoiesis—the process of red
blood cell production. Anemia, a prevalent hematologic complication in HIV-infected
individuals, often serves as a marker of disease progression and impacts overall health
outcomes. This paper aims to delve into the intricate relationship between HIV-associated
bone marrow alterations and their consequential effects on erythropoiesis. The mechanisms
underlying bone marrow changes in HIV infection, including direct viral effects,
dysregulation of cytokine networks, and inflammatory processes, significantly disrupt the
delicate balance necessary for efficient erythropoiesis. The impact of these alterations on
erythropoiesis manifests through ineffective red blood cell production, decreased
erythropoietin responsiveness, and shortened red blood cell lifespan. Chronic inflammation
further complicates erythropoietic processes, contributing to the development and
perpetuation of anemia in HIV-infected individuals. Therapeutic interventions encompass a
multifaceted approach, including antiretroviral therapy (ART) to control viral replication,
erythropoiesis-stimulating agents, and adjunctive nutritional support to manage anemia.
However, emerging research targeting bone marrow microenvironmental factors and novel
agents stimulating erythropoiesis offer promising avenues for future therapeutic
development.
Keywords: HIV, bone marrow, erythropoiesis, erythropoietin, antiretroviral therapy