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Updated: Feb 8, 2026

Plaquing of Herpes Simplex Viruses
Published on: November 5, 2021
Immuno-metabolic changes in herpes virus infection
Debprasad Chattopadhyay1, Aparna Mukhopadhyay2, Durbadal Ojha3
1ICMR-National Institute of Traditional Medicine, Nehru Nagar, Belagavi 590010, India; ICMR-Virus Unit, Infectious Diseases and Beliaghata General Hospital, 57 Dr Suresh Chandra Banerjee Road, Beliaghata, Kolkata, West Bengal 700010, India.
Cellular metabolism impacts immune responses to Herpes simplex virus (HSV). Metabolic shifts influence immune cells and cytokines, affecting HSV infection, pathogenesis, and control.
Area of Science:
- Immunology
- Virology
- Metabolomics
Background:
- Cellular metabolic pathways significantly influence host immune responses and overall health.
- Human Herpes simplex virus types 1 and 2 (HSV-1, HSV-2) cause a spectrum of diseases, from mild herpes to severe neurological complications.
- Immune responses to HSV involve intricate interactions between innate and adaptive immunity, including Interferon-1 (IFN-1) induction and the roles of Natural Killer (NK) cells and plasmacytoid Dendritic Cells (pDC).
Purpose of the Study:
- To review the critical role of the metabolome in modulating innate and adaptive immune responses during HSV infection.
- To highlight the interplay between metabolic alterations and immune system function in the context of HSV pathogenesis and control.
- To discuss how viral proteins, such as ICP0, interfere with host immune signaling pathways.
Main Methods:
- Literature review synthesizing current evidence on metabolomics and HSV immunity.
- Analysis of studies detailing metabolic pathway alterations in HSV-infected hosts.
- Examination of research on immune cell function and cytokine profiles in relation to metabolic changes during HSV infection.
Main Results:
- Metabolic changes demonstrably affect the up- or down-regulation of key cytokines and chemokines (e.g., IFN-γ, IL-2, IL-4, IL-10, MIP1β) during HSV infection and recurrence.
- The viral protein ICP0 is identified as a key factor that attenuates Toll-like receptor (TLR) signaling, thereby inhibiting innate immune responses to HSV.
- Metabolomic alterations are linked to the efficacy of both innate and adaptive immune effectors in controlling HSV infection and establishing latency.
Conclusions:
- The metabolome plays a crucial role in shaping the immune landscape during HSV infections.
- Understanding metabolic reprogramming in HSV infection is vital for developing novel therapeutic strategies.
- Targeting metabolic pathways could offer new avenues for enhancing anti-HSV immunity and managing disease recurrence.
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