From the Guidelines
Retroviral infection pathophysiology involves a complex process of viral replication and integration into the host genome, leading to the depletion of CD4+ T cells and immunodeficiency, as seen in HIV infection 1. The pathophysiology of retroviral infection can be broken down into several key steps:
- Entry into the host cell through specific receptor binding
- Reverse transcription of viral RNA into DNA using the enzyme reverse transcriptase
- Integration of the viral DNA into the host cell's genome using the enzyme integrase
- Transcription of viral genes and production of new viral proteins and RNA genomes
- Assembly and budding of new viral particles from the host cell membrane This process allows the virus to persist indefinitely in infected cells, creating a permanent viral reservoir, and enables retroviruses to rapidly evolve and evade immune responses 1. The depletion of CD4+ T cells is a major clinical finding in progressive HIV infection, and is associated with increased clinical complications and immunodeficiency 1. Key factors that influence the pathophysiology of retroviral infection include:
- Viral load: the amount of viral RNA in the blood
- CD4+ T cell count: the number of CD4+ T cells in the blood
- The presence of opportunistic infections and other clinical complications Understanding the pathophysiology of retroviral infection is crucial for the development of effective treatments and prevention strategies, and for improving patient outcomes and quality of life 1.
From the Research
Pathophysiology of Retroviral Infection
The pathophysiology of retroviral infection involves several key steps, including:
- Viral entry into the host cell
- Reverse transcription of the viral genome
- Integration of the viral DNA into the host chromosome
- Transcription and translation of the viral genes
- Assembly and release of new virus particles
Integration of Viral DNA
The integration of viral DNA into the host chromosome is a critical step in the retroviral life cycle, and is mediated by the viral enzyme integrase 2, 3, 4. This process involves the cutting and joining of DNA strands, and results in the formation of a stable proviral genome. The integrase enzyme is a key target for antiretroviral therapy, and inhibitors of this enzyme have been shown to be effective in blocking viral replication 2, 4.
Host-Cell Barriers to Infection
The host cell has several barriers to retroviral infection, including structural components and specific antiretroviral activities 5. Retroviruses have evolved auxiliary factors that promote infectivity by overcoming these barriers, and these factors play a critical role in the viral life cycle.
Consequences of Infection
The consequences of retroviral infection can be severe, and include the disruption of host cell function, the activation of proto-oncogenes, and the acquisition of oncogenes 3. The progressive loss of CD4+ T cells is a hallmark of HIV infection, and can ultimately lead to the development of acquired immune deficiency syndrome (AIDS) 6. The monitoring of CD4+ T cell counts is an important tool for tracking disease progression and the effectiveness of antiretroviral therapy 6.