Abstract :
The coexistence of Sickle Cell Disease (SCD) and Human Immunodeficiency Virus (HIV) infection presents a unique
and complex clinical challenge due to the intricate interplay between chronic hemolytic anemia, immune
dysregulation, and viral replication. SCD is characterized by chronic inflammation, functional asplenia, and frequent
blood transfusions, all of which contribute to an altered immune environment that may influence HIV viral load
dynamics. Conversely, HIV-induced immunosuppression can exacerbate SCD complications, increasing
susceptibility to infections and organ damage. Understanding how these two conditions interact is essential for
optimizing viral suppression and managing hematological complications in co-infected individuals. Antiretroviral
therapy (ART) remains the cornerstone of HIV management, but its effectiveness in SCD patients can be
compromised by factors such as chronic inflammation, drug toxicity, and transfusion-related complications. Certain
ART regimens, especially those with hematologic side effects, may worsen anemia and bone marrow suppression in
SCD patients, complicating adherence and viral load control. Additionally, blood transfusions, a common intervention
in SCD, can trigger immune activation and iron overload, potentially affecting ART pharmacokinetics and viral replication. These challenges necessitate personalized treatment strategies that balance effective HIV suppression
with the management of SCD-related complications.
Keyword :
Viral Load, Sickle Cell Disease, HIV, Antiretroviral Therapy, Immune Response