The gut microbiome can have a significant impact on the acquisition of Epstein-Barr virus (EBV) and human immunodeficiency virus-1 (HIV) infection and also plays a role in the course of the disease, finds a new study, challenging previous research that shows a protective effect.

Recent research has shown that the bacteria and other microbes in our gut play a supporting role in immunity, metabolism, digestion, and the fight against "bad bacteria" that try to invade our bodies.

However, using a first-of-its-kind precision experimental model with no microbiome (germ-free), the research published in Nature Biotechnology showed may the gut microbiome may not be as always protective against human pathogens.

"These findings offer the first direct evidence that resident microbiota can have a significant impact on the establishment and pathology of infection by two different human-specific pathogens," said Angela Wahl, assistant professor at the University of North Carolina’s Department of Medicine.

In the study, the team compared the conventional humanised experimental model to one that was humanised and free of bacteria.

HIV is a retrovirus that primarily infects human CD4+ T cells and is mainly acquired through the GI tract. Rectal exposure, for example, in men who have sex with men accounts for more than half of new HIV infections. Breastfeeding is an example of oral exposure that can also transmit HIV to infants.

Dr Wenbo Yao, the co-first author, found that rectal HIV acquisition was 200 per cent higher in experimental models colonised with resident microbiomes compared to germ-free experimental models. 

Similarly, oral HIV acquisition was 300 per cent higher in experimental models colonised with resident microbiota compared to germ-free experimental models.

Researchers also noticed that experimental models colonised with resident microbiota had HIV-RNA levels that were up to 34 times higher in plasma and more than 1,000 times higher in tissues than germ-free experimental models.

Further, they then performed comparisons between colonised and germ-free experimental models, which revealed that the presence of resident microbiota increased the frequency of CCR5+CD4+ T cells, which are the main target of HIV infection throughout the gut. 

The findings suggest that enhanced HIV acquisition and replication is due to, at least in part, an increased density of target cells for local infection following oral or rectal HIV exposure.

The findings on EBV were also important. EBV is a DNA herpes virus that infects B cells and can cause mononucleosis. Almost 95 per cent of the adult population harbours latent infection of EBV but for some people with compromised immune systems. 

EBV infection can influence the development of certain types of cancers such as Hodgkin’s lymphoma, Non-Hodgkin lymphoma, Burkitt’s lymphoma and Nasopharyngeal carcinoma.

The team found that an experimental model with a normal microbiome that was exposed to EBV developed large macroscopic tumours in a variety of organs, including the spleen, liver, kidney, and stomach. These tumours were virtually absent in the germ-free experimental model infected with EBV.