The latest research says herpes virus goes On and Off
Herpes is a common viral infection that affects millions of people worldwide. The herpes simplex virus (HSV) can cause painful blisters and sores, typically on the lips, mouth, or genitals. The virus can hide in the body’s nerve cells. It can lie dormant for some time. Eventually, it may reactivate and cause outbreaks. This constant ebb and flow of infection has puzzled researchers for decades. Recent studies have shed new light on these mechanisms.
Understanding the life cycle of the herpes virus
During the initial infection, the virus travels along the nerves to the nerve ganglia, where it enters a latency period. The virus remains inactive in this state, and only a few genes are expressed. The virus can remain latent for years, even decades, without causing symptoms.
However, the virus can reactivate anytime, often triggered by stress, illness, or sun exposure. When the virus is reactivated, it travels back to the skin via the nerves and causes blisters and sores. The virus can also be shed through the skin without causing visible symptoms, possibly transmitting the infection to others.
Recent advances in understanding viral latency
One of the most important breakthroughs in understanding herpes latency came from a study published in Nature Communications in May 2024.
Researchers at the Fred Hutchinson Cancer Center in Seattle used gene editing technology. They eliminated up to 97% of the herpes virus in mouse models of oral and genital herpes.
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In experimental gene therapy, a mixture of gene-editing molecules is injected into the bloodstream. This mixture includes a vector used in gene therapies and enzymes that act as molecular scissors. The vector delivers the enzymes to nerve centres where the herpes virus is located. The scissors cut the virus’s DNA, damaging it irreparably.
“We use a meganuclease enzyme,” says Martine Aubert, PhD. She is a senior scientist at Fred Hutch and the study’s lead author. “This enzyme cuts at two different sites in the virus’s DNA. “These cuts damage the virus so much that it can’t repair itself. The body’s repair systems recognize and eliminate the damaged DNA as foreign.”
The researchers found that gene therapy reduced the frequency and amount of viral shedding. This suggests it could also lower the spread of the virus. This is important for people with herpes, who often worry about spreading the infection to their partners.
Another study, published in the Journal of Virology in November 2022, examined herpes reactivation. Researchers discovered that a protein called ICP0 is crucial for the virus to move from latency to an active state.
During latency, the herpes virus suppresses the expression of ICP0 to avoid detection by the host’s immune system. However, when the virus reactivates, ICP0 levels increase. This increase allows the virus to express its genes and produce new particles.
The influence of stress on the immune system
Stress is a known trigger for herpes outbreaks, and recent research has shed light on the mechanisms behind this link. A study published in the Journal of Immunology in February 2024 found that stress hormones can suppress the body’s immune response to the herpes virus.
The researchers exposed mice to stressful conditions and found that their levels of stress hormones, such as corticosterone, increased. This led to decreased natural killer (NK) cell activity, which is essential for fighting herpes infections.
When the stressed mice were infected with HSV-1, they experienced more severe symptoms and higher viral replication than non-stressed mice. These results suggest that stress-induced suppression of the immune system may be a critical factor in the reactivation of herpes.
The immune system also plays a crucial role in controlling herpes infections during latency. A study published in the Journal of Experimental Medicine in January 2024 found that tissue-resident memory (TRM) T cells are crucial for preventing herpes reactivation. These cells are vital for controlling the virus in the skin.
TRM cells are located in the skin and mucous membranes. They provide immediate protection against pathogens. The study found that TRM cells specific to HSV-1 were present in the skin of infected mice, even during latency.
When TRM cells were depleted in the mice, the animals had more frequent and severe herpes outbreaks. This suggests that TRM cells are crucial for controlling the virus. Understanding their role in herpes latency could lead to new strategies to boost the immune response to the virus.
The link between herpes and Alzheimer’s disease
Recent research links herpes to an increased risk of Alzheimer’s disease. A study published in the Journal of Alzheimer’s Disease in July 2024 found this connection. People who have been infected with herpes are twice as likely to develop dementia compared to those who have never been infected.
The researchers used imaging techniques to examine the brains of people with and without herpes. They found more inflammation and damage in brain regions related to Alzheimer’s in those with a history of herpes.
More research is needed to understand this link fully. However, the findings suggest that herpes might contribute to Alzheimer’s by causing chronic brain inflammation.
This highlights the importance of controlling herpes infections and preventing reactivation to reduce the risk of long-term neurological complications.
Current and future treatments for herpes
There is currently no cure for herpes. Several antiviral medications are available to relieve symptoms. These include acyclovir, valacyclovir, and famciclovir.
However, these drugs only suppress the active, lytic phase of the virus. They do not eliminate the virus from its latent state in nerve cells. This is why people with herpes often have recurring outbreaks.
Researchers are developing new treatments to target the virus during latency. The goal is to achieve a functional cure. One promising approach is gene editing technology, similar to the method used in the Fred Hutch study.
Another potential treatment involves small interfering RNAs (siRNAs). SiRNAs can silence specific viral genes. This helps prevent the virus from reactivating. A study in the Journal of Virology in March 2024 found that siRNAs targeting the ICP0 gene reduced herpes reactivation in cell culture experiments.
Researchers are also looking into therapeutic vaccines. These vaccines aim to boost the body’s immune response to the herpes virus. They are designed to stimulate antibodies and T-cells specific to HSV. This could help control the infection and prevent reactivation.
Several clinical trials are underway to test these new treatments. If successful, they could significantly improve the quality of life for people with herpes. They may also reduce the transmission of the virus to others.
Read more: Finding Hope: Positive Aspects of Dating With Herpes
Conclusion
The herpes simplex virus can hide in nerve cells. It can reactivate at any time. This leads to painful outbreaks and possible transmission to others. Recent research offers new insights into why the virus behaves this way. It looks at gene editing, stress hormones, and the immune system.
Currently, there is no cure for herpes. However, new treatments are being developed. These include gene editing technology, small interfering RNAs, and therapeutic vaccines. These treatments target the virus during latency and provide a functional cure.
As research progresses, people with herpes need to work closely with their healthcare providers. This helps manage symptoms and reduce transmission risk. With the proper treatment and proper support, people with herpes can lead healthy and fulfilling lives.