Understanding host-virus interactions is crucial for developing effective treatments and vaccines for chronic viral infections.

Chronic viral infections such as HIV, HBV, and HCV manipulate host immune responses through various mechanisms, including antigenic variation and cytokine dysregulation.

These viruses employ strategies like downregulating MHC class I and disrupting interferon signaling to evade the immune system.

Additionally, they induce epigenetic changes in infected cells, which modulate gene expression and further enhance immune evasion.

Persistent infections lead to T cell exhaustion, characterized by increased expression of inhibitory receptors like PD-1, ultimately reducing T cell function.

The immunosuppressive environment created by chronic viral infections is driven by cytokines such as IL-10 and TGF-β, which inhibit T cell activation.

Key viral proteins, including HIV Nef, HBV X protein, and HCV NS5A, disrupt immune responses by interfering with antigen presentation and cytokine signaling.

To combat these challenges, therapeutic strategies under consideration include immune checkpoint inhibitors, cytokine treatments, and CRISPR technology aimed at enhancing antiviral responses.