Nikhil Prasad Fact checked by:Thailand Medical News Team May 29, 2026 7 hours, 14 minutes ago
Medical News: For years, scientists have believed that Ebola virus primarily spreads through direct contact with infected bodily fluids and that the skin serves largely as a protective barrier separating the virus from the outside world. However, a new study is overturning that assumption by revealing that the skin may play a far more active role in Ebola virus disease than previously recognized. Researchers have discovered that Ebola virus can infect skin tissue, accumulate there during the course of infection, travel through specific skin structures, and potentially use the skin as both a route of viral entry and a pathway for transmission to others.
Scientists have discovered that Ebola virus actively infects skin tissue and may use hair follicles and damaged
skin as pathways for transmission and spread
The findings are particularly significant because Ebola virus remains one of the World Health Organization's top global health threats despite the availability of approved vaccines. The study provides new insights into how the virus behaves within the body and raises important questions about transmission risks during outbreaks.
The research was conducted by scientists from the University of Iowa, Texas Biomedical Research Institute, Boston University, the Galveston National Laboratory at the University of Texas Medical Branch, and the University of California. Their work challenges long-standing assumptions about Ebola virus disease and identifies the skin as an unexpectedly important target organ during infection.
Ebola Found to Build Up in Skin During Infection
Using samples from Ebola-infected non-human primates and several mouse models, the researchers carefully tracked how the virus spread through the body over time. They found that viral loads within the skin increased steadily as infection progressed.
Importantly, skin infection was not limited to the area where the virus initially entered the body. Viral material was detected in skin located far from the original infection site, indicating that Ebola can disseminate throughout the body and eventually establish infection in distant skin tissues.
The investigators observed that skin infection generally occurred later than infection of major internal organs such as the liver and visceral fat. Nevertheless, once the virus reached the skin, viral levels continued to rise, demonstrating that skin tissue actively supports viral replication rather than merely harboring virus transported from other organs.
Hair Follicles May Serve as Viral Escape Routes
Among the most intriguing findings was the discovery that Ebola virus frequently localized around hair follicles and associated skin structures.
Researchers detected viral proteins in cells surrounding hair follicles as well as in epithelial cells lining these structures. This observation suggests that hair follicles may provide a pathway that allows Ebola virus to move from deeper layers of skin toward the outer surface.
The study authors believe this may represent a previously unrecognized mechanism through which infectious virus reaches the skin surface. Such a mechanism could help
explain earlier reports from Ebola outbreaks in which infectious virus and viral genetic material were detected on the skin of infected individuals.
The possibility that hair follicles contribute to viral shedding introduces an entirely new dimension to understanding Ebola transmission dynamics.
Extensive Infection Occurs with Surprisingly Little Inflammation
One of the study's most unexpected findings was the apparent disconnect between viral burden and inflammation within skin tissue.
In organs such as the liver and visceral fat, infection triggered robust inflammatory responses characterized by increased expression of multiple immune-related genes. However, the skin behaved very differently.
Despite substantial viral loads and widespread infection of skin cells, researchers found minimal evidence of significant inflammatory activity. Important inflammatory markers remained largely unchanged even when viral antigen was readily detectable throughout the skin.
This unusual immune response may provide Ebola with a favorable environment in which to replicate while avoiding detection. Scientists believe the lack of strong inflammation could allow infected skin to act as a relatively silent viral reservoir during advanced stages of disease.
This
Medical News report notes that such findings may help explain why infectious virus can persist on the skin without producing obvious visible signs of severe skin inflammation.
Infection Appears in Patchy Viral Hotspots
The researchers also discovered that Ebola infection within skin tissue is highly uneven.
Instead of spreading uniformly throughout the skin, the virus formed concentrated clusters or "hotspots" of infection. Some regions contained high levels of infectious virus while neighboring areas remained largely unaffected.
This patchy pattern was observed repeatedly in both primate and mouse models. The finding helps explain why virus detection from skin samples can sometimes be inconsistent and suggests that localized pockets of infection may serve as important sources of viral shedding.
Scientists identified infected immune cells, stromal cells, endothelial cells, macrophages, fibroblast-like cells, and epithelial cells within these hotspots, highlighting the broad range of skin cell types susceptible to Ebola infection.
Damaged Skin Can Become a Gateway for Infection
Perhaps the most concerning finding involved the ability of Ebola-like viruses to enter the body through damaged skin.
When researchers gently removed the outer protective layer of skin and applied a surrogate Ebola virus to the exposed surface, infection rapidly developed within epidermal cells. In some animals, the infection subsequently spread to internal organs including the spleen and liver.
Animals exposed through abraded skin experienced significant illness and, in some cases, death. By contrast, intact skin provided much greater protection against systemic infection.
These observations suggest that cuts, abrasions, scratches, and other disruptions of the skin barrier may significantly increase the risk of infection following exposure to contaminated materials.
AXL Receptor Identified as a Key Player
The study also identified the phosphatidylserine receptor AXL as an important factor in Ebola skin infection.
Experiments showed that animals lacking AXL experienced significantly reduced infection within skin tissues. The receptor appears to help facilitate viral entry into skin cells and may play a particularly important role during the earliest stages of infection.
This finding raises the possibility that therapies targeting AXL-related pathways could eventually help reduce Ebola infection at the skin level.
Conclusions
The study fundamentally reshapes current understanding of Ebola virus pathogenesis by establishing the skin as an active participant in infection rather than a passive barrier. The findings demonstrate that Ebola virus can replicate extensively within skin tissue, infect multiple skin cell populations, exploit hair follicles as potential routes to the skin surface, and establish infection with remarkably little inflammation. Equally important, damaged skin can serve as a portal of entry capable of initiating systemic disease. Together, these discoveries have major implications for outbreak control, healthcare worker protection, infection-prevention strategies, patient management, and future therapeutic development. As researchers continue to investigate how these mechanisms operate in humans, the skin may emerge as a critical target for interventions designed to reduce Ebola transmission and disease severity.
The study findings were published in the peer reviewed Journal of Virology.
https://journals.asm.org/doi/10.1128/jvi.01300-25
For the latest Ebola news, keep on logging to Thailand
Medical News.
Read Also:
https://www.thailandmedical.news/articles/ebola
Share
Tweet
Share
