Nikhil Prasad Fact checked by:Thailand Medical News Team Jan 09, 2025 12 hours, 51 minutes ago
Medical News: Recent research led by scientists from the University of Brescia and the University of Calabria has uncovered critical insights into how Human Metapneumovirus (HMPV), a common respiratory virus, interacts with the human immune system. This virus, known for causing respiratory illnesses ranging from mild colds to severe pneumonia, appears to establish a persistent infection in the endothelial cells of the lungs, potentially contributing to chronic immune issues.
Persistence of Human Metapneumovirus and Its Role in Th2 Immune Skewing
This
Medical News report sheds light on findings that not only highlight the resilience of HMPV but also its ability to alter immune responses in the human body. The study also provides a detailed examination of the cellular mechanisms involved in HMPV infections and their implications for long-term respiratory health.
The Persistent Nature of HMPV
HMPV is an RNA virus closely related to the respiratory syncytial virus (RSV). It primarily targets the respiratory system and can cause significant health concerns, especially in young children, the elderly, and immunocompromised individuals. According to the study, HMPV does not merely invade and replicate within host cells; it persists in lung microvascular endothelial cells for over 30 days without causing noticeable damage. This persistence ensures the virus’s continuous release, maintaining its presence in the lung microenvironment.
Endothelial cells in the lung, which line the inner walls of blood vessels, appear to act as reservoirs for the virus. Unlike epithelial cells, which show visible damage during viral infections, endothelial cells harbor the virus in a non-destructive manner, allowing its long-term survival and propagation.
How HMPV Alters the Immune System
The study found that during its persistent infection, HMPV primes the immune system toward a Th2-skewed response. In simpler terms, the virus subtly manipulates the body’s immune defense to favor a type of response less effective at eliminating viral infections. This manipulation could explain why some individuals struggle to fully clear the infection or develop chronic respiratory issues like asthma following an HMPV infection.
Researchers observed that HMPV-infected endothelial cells release viral particles capable of interacting with dendritic cells. Dendritic cells are essential for initiating immune responses, but exposure to HMPV particles altered their behavior. These dendritic cells, when exposed to naïve CD4 T-cells, promoted their differentiation into Th2-type cells. Th2 cells are typically associated with allergic responses and asthma, rather than the strong antiviral responses needed to combat HMPV.
The Role of OX40L in Immune Skewing
One of the study’s most significant findings was the role of a specific molecule, OX40L, in this immune skewing process. OX40L, present on the surface of dendritic cells, was upregulated when these cells interacted with HMPV particles.<
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This upregulation was directly linked to the promotion of a Th2-type immune response. Blocking OX40L in laboratory experiments effectively reversed the Th2 skewing, suggesting it as a potential therapeutic target for controlling HMPV-induced immune changes.
Broader Implications of the Study
The discovery that endothelial cells can serve as long-term reservoirs for HMPV challenges previous assumptions that respiratory infections are limited to short-term impacts. It also raises questions about the potential role of these infections in chronic lung diseases. This study highlights the need for further research into the long-term effects of viral infections on immune system functioning and their contributions to diseases like asthma and chronic obstructive pulmonary disease (COPD).
Additionally, understanding the mechanisms by which HMPV persists and alters immune responses could pave the way for novel treatments. Targeting molecules like OX40L might help mitigate the long-term immune effects of HMPV and improve outcomes for patients with severe respiratory infections.
Study Methodology and Key Findings
The research team employed cutting-edge laboratory techniques to study the interactions between HMPV, endothelial cells, and dendritic cells. Key highlights from their work include:
-Persistent Infection: HMPV was found to replicate and release viral particles from endothelial cells for over a month without causing cell death or damage.
-Immune Skewing: Viral particles released from infected cells primed dendritic cells to promote a Th2-type immune response, marked by increased production of IL-4, a cytokine associated with allergic reactions.
-Role of OX40L: The expression of OX40L on dendritic cells was critical in directing the Th2-skewed immune response. Neutralizing OX40L reversed this effect, suggesting its pivotal role in the process.
-Impact of Viral Particles: Even inactivated HMPV particles could replicate these immune-modulating effects, emphasizing the virus’s ability to influence immune responses without active replication.
Conclusion
This groundbreaking study reveals how HMPV establishes persistent infections and alters the immune system, potentially contributing to chronic respiratory conditions. The findings underscore the importance of continued research into viral mechanisms and their long-term impacts on health. Future studies could explore therapeutic interventions targeting molecules like OX40L to mitigate the adverse immune effects of persistent viral infections.
The study findings were published in the peer-reviewed journal: Microorganisms.
https://www.mdpi.com/2076-2607/8/6/824
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https://www.thailandmedical.news/articles/hmpv-human-metapneumovirus
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