negative regulation of defense response to virus by host

Definition

Target type: biologicalprocess

Any host process that results in the inhibition of antiviral immune response mechanisms, thereby facilitating viral replication. The host is defined as the larger of the organisms involved in a symbiotic interaction. [GOC:ai, GOC:dph, GOC:tb]

Negative regulation of defense response to virus by host is a complex biological process that involves a variety of cellular and molecular mechanisms designed to prevent excessive or inappropriate immune responses to viral infections. Here's a detailed breakdown:

1. **Viral Recognition:** The host's immune system relies on pattern recognition receptors (PRRs) to detect viral components like double-stranded RNA (dsRNA) or viral DNA. PRRs are expressed by cells of the innate immune system, such as macrophages, dendritic cells, and natural killer (NK) cells.

2. **Signaling Cascades:** Upon viral recognition, PRRs trigger signaling cascades that activate transcription factors like interferon regulatory factors (IRFs) and nuclear factor kappa B (NF-κB). These transcription factors induce the production of type I interferons (IFNs), pro-inflammatory cytokines, and other antiviral proteins.

3. **Antiviral Response:** IFNs bind to specific receptors on neighboring cells, initiating a cascade of events that renders them resistant to viral infection. These antiviral responses include:
- **Inhibition of viral replication:** IFNs can block viral protein synthesis, inhibit viral gene expression, and degrade viral RNA.
- **Enhancement of MHC class I expression:** Increased MHC I expression allows infected cells to display viral antigens, leading to their recognition and destruction by cytotoxic T lymphocytes (CTLs).
- **Activation of NK cells:** IFNs enhance the cytotoxic activity of NK cells, which can directly kill infected cells.

4. **Negative Regulation:** While a robust immune response is crucial for virus control, excessive inflammation can damage host tissues and contribute to disease pathology. Therefore, negative regulatory mechanisms are essential to prevent overactivation of the immune response and maintain homeostasis. These mechanisms include:
- **Suppression of IFN signaling:** Viral proteins can target and inhibit various components of the IFN signaling pathway, including the JAK-STAT pathway and downstream effector molecules.
- **Induction of immunosuppressive cytokines:** Some viruses can induce the production of immunosuppressive cytokines like IL-10, which dampen the immune response and promote viral persistence.
- **Expression of decoy receptors:** Some viruses express proteins that mimic the structure of IFN receptors, acting as decoys to bind and neutralize IFNs.
- **Inhibition of antigen presentation:** Some viruses can interfere with the processing and presentation of viral antigens to CTLs, hindering the development of a specific adaptive immune response.

5. **Viral Evasion Strategies:** Viruses have evolved sophisticated mechanisms to evade the host immune system. These strategies include:
- **Mutation and antigenic drift:** Viruses can undergo rapid mutation, generating new variants that escape recognition by the host's adaptive immune system.
- **Immune suppression:** Some viruses actively suppress the immune response by targeting immune cells or inhibiting immune signaling pathways.
- **Latency:** Some viruses can establish a latent state within the host, evading the immune system until conditions are favorable for reactivation.

6. **Host-Virus Coevolution:** The ongoing battle between host and virus has shaped the evolution of both. Hosts have developed complex immune systems to combat viruses, while viruses have evolved strategies to evade these defenses. This coevolutionary arms race ensures the survival of both host and virus.

In summary, negative regulation of defense response to virus by host involves a delicate balance between activating an effective immune response and preventing excessive inflammation. Viruses have evolved numerous strategies to manipulate and evade host immune defenses, creating a constant evolutionary arms race.'
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Proteins (1)

Compounds (2)