Researchers have made a significant breakthrough in the fight against herpes infections by developing a mini-antibody, or nanobody, that neutralizes a key protein essential for the infection. This novel intervention would provide unprecedented protection from HSV-1 and HSV-2 to millions of at-risk individuals. We can protect those who are most susceptible to these potentially deadly viruses. Approximately 60% of the population has HSV-1, and 20% of the population has genital herpes (with genital herpes primarily caused by HSV-2). This further emphasizes the critical need for highly effective treatments.
While HSV-1 usually appears as painful skin sores on the face like cold sores, HSV-2 is most often the cause of genital herpes. Both HSV and CMV depend on a protein known as glycoprotein B (gB) to invade host cells. To create the new nanobody, scientists used the immune response of an alpaca named Max. This nanobody holds promise for walling off viruses from effectively infecting cells. Such a breakthrough in discovery would be transformative towards developing therapies targeted to those at risk. Newborns, in particular, are in great jeopardy during birth if their mothers bear current herpes infections.
Understanding Herpes and Its Impact
Herpes Simplex Virus, while stigmatized, is a common infection that impacts millions of people around the world. Based on our latest estimates, over 40 million people are newly infected with herpes annually. The two main strains, HSV-1 and HSV-2, pose different yet important challenges within the realm of public health. HSV-1 is primarily responsible for cold sores, but can cause genital infections. In contrast, HSV-2 is the primary cause of genital herpes.
These viruses are transmitted through direct skin-to-skin contact or contact with mucous membranes. Viral entry The early stage of infection consists of the virus attaching itself to the cell membrane of infected hosts. Once gB attaches, it makes a dramatic 180-degree flip in its three-dimensional structure. This key change allows the virus to effectively fold and disrupt the host cell membrane, allowing the viral RNA to enter. This process eventually permits the virus to “sneeze,” or inject its contents into the host cells, thus beginning infection.
Public health campaigns are increasing pressure to inform people. To address the virus’s high prevalence, largely through prevention and treatment options, they’ve shifted to focus on the nonmedicinal aspects of care. Current antiviral treatments mostly reduce severity and duration but do not clear the virus from the body. Ongoing research into novel treatments is crucial to improving the quality of life of those living with herpes. The nanobody that we have just developed holds great promise in this regard.
The Development of the Nanobody
A collaborative of scientists led significant and innovative research efforts to develop that nanobody. Their goal was to find new therapeutic strategies to fight herpes infections. And so they went in search of an alpaca named Max. In fact his immune system produced antibodies that were superstars in homing in on gB.
In order to start up this cascade, Max was vaccinated with a gB protein subunit. This immunization elicited an immune response resulting in generation of highly specific antibodies. With those unique signatures in hand, the researchers isolated and characterized the antibodies. Ultimately, they screened 6,500 nanobodies to locate one that binds gB with incredible affinity.
Even more important was the timing of this discovery with respect to when researchers unveiled the 3D structure of native HSV-2 gB. They did this phenomenal work thanks to a Hamburg nanobody. Appreciating this ultimately structural relationship helps explain why the nanobody is so effective. More importantly, it opens up exciting new research and development opportunities.
Mechanism of Action and Future Implications
Additionally, the nanobody is able to bind to prefusion gB, thus neutralizing the herpes virus’s ability to infect host cells. By blocking this critical step in the viral entry process, it provides a very promising therapeutic intervention at this critical nexus. This possible mechanism suggests exciting new possibilities for building new strategies. Improve protection of those at risk for HSV acquisition and decrease the rate of recurrent outbreaks among those already infected.
The impact of this research goes well beyond treatment as it opens doors to preventative opportunities. An example of this is that pregnant women with active herpes infections can have significant risk to their newborns at delivery. Developing an effective therapeutic agent that can neutralize the virus would significantly decrease this risk. It would have the dual effect of hugely saving neonatal lives.
Researchers are in ongoing lab and clinical studies engaged in further improving and testing the nanobody’s efficacy. This progress inspires cautious optimism about the law’s potential to positively impact public health. The ability to neutralize both HSV-1 and HSV-2 expands its applicability and raises hopes for a comprehensive approach to managing herpes infections.