In a recent study, scientists from the NIH identify a set of protein complexes that are recruited viral genes and stimulate not only initial HSV infection, but also reactivation of dormant HSV.
Herpes simplex virus (HSV) is one of the most prevalent sexually transmitted diseases. Most individuals who have genital herpes are unaware of their infection, and to make matters worse, once infected, the virus is known to periodically reactivate after years of remaining dormant. Not much is known about this problematic cycle, which leaves us at a severe disadvantage in the fight against the virus, especially since once someone is infected with herpes—they have it for life.
Due to this, researchers everywhere have been working hard to learn more about the virus. In fact, scientists from the National Institutes of Health were recently able to identify “a set of protein complexes that are recruited to viral genes and stimulate both initial infection and reactivation from latency,” according to the press release. They also found that “environmental stresses known to regulate these proteins also induce reactivation.”
Genital herpes is caused by two types of viruses: herpes simplex type 1 (HSV-1) and herpes simplex type 2 (HSV-2). According to the World Health Organization, 500 million individuals are infected with HSV-2 on a global scale, and two-thirds of the population are infected with HSV-1. These viruses can result in several complications, ranging from oral cold sores to genital lesions to serious eye conditions that could potentially lead to complete loss of vision. Not only that, but those infected with HSV are at increased risk of getting or transmitting HIV.
When it comes to infants, HSV is even known to result in neurological or developmental complications. For example, what may have been the first immunological evidence that mothers who experience active genital herpes infections during early pregnancy may be more likely to have offspring that will later be diagnosed with autism spectrum disorders has recently been presented by researchers from Columbia University’s Mailman School of Public Health in collaboration with researchers from the Norwegian Institute of Public Health.
This study built off of previous findings that shed light on the role that a cellular protein called HCF-1 plays in the initiation and reactivation of HSV infection. So, what does HCF-1 do? Researchers found that HCF-1, along with other associated proteins, “are recruited to the viral genome to enable the virus to replicate and spread.” In addition, this work also yielded “targets for the development of therapeutics to suppress infection and reactivation.”
Now, in the new study, the NIH, in collaboration with researchers from Princeton University, has managed to take the research a step further by identifying “new HCF-1 protein complexes that play additional roles” in the initiation and reactivation of viral infection. In a mouse model, the researchers found that by using “compounds that turn on components of these HCF-1 protein complexes,” they could reactivate dormant HSV infection. Furthermore, their findings suggest that HCF-1 associated proteins also play a role in the reactivation of dormant HIV.
So, what’s next in this line of research? According to the press release, “The researchers are continuing to investigate the protein complexes involved in promoting HSV gene expression, infection, and reactivation from latency. Identifying these complexes and understanding the mechanisms by which they function can potentially reveal additional targets for the development of new therapeutics.”