The majority of individuals newly infected with HIV-1 develop a transient symptomatic illness, associated with high levels of HIV-1 replication and an expansive antiviral immune response.

It is during this initial cycle of viral replication that important pathogenic processes are thought to occur. These include the seeding of virus to a range of tissue reservoirs and the destruction of CD4+ T lymphocytes, in particular within the lymphoid tissues of the gut.

The very high levels of HIV-1 viremia are normally short-lived, indicating that the host is able to generate an immune response that controls viral replication. Over the following weeks, viremia declines by several orders of magnitude before reaching a setpoint point of viral replication that is a strong predictor of the speed of HIV-1 disease progression.

Several factors can influence viral replication during acute infection and the establishment of a viral setpoint, including the fitness of the infecting virus, host genetic factors and host immune responses. This initial phase of the infection therefore represents an ideal scenario to investigate and identify the correlates of protective immunity in HIV-1 infection.

The overall goal of the Acute HIV-1 Infection research efforts at the Ragon Institute is to define predictable elements of the virus-host interaction that occur during acute HIV infection, and exploit these to guide effective HIV vaccine design. 

Website: Acute HIV Infection Research Program

Laboratories which focus on Acute HIV-1 Infection:
		Allen Lab
		Altfeld Lab
		Le Gall Lab
		Walker Lab
		Yu Lab
Research Coordinator:
		Karen Axten, Project Coordinator phone: 617.726.2306