1/26/2024 0 Comments Hsv cure found in india![]() “It’s an interesting observation,” he tells The Scientist. He explains that black 6 mice in particular have differently structured immune systems than other lab mice that could have contributed to this effect. Kastrukoff adds that the young age of the mice (5 weeks), the type of HSV-2, and the strain of mouse (C57BL/6 or “black 6,” a common inbred lab mouse) in the study could all have contributed to the atypical results. In mice, however, Koelle says the virus travels up the spinal cord and into the brain, which is what causes the animals’ eventual deaths. ![]() In humans, the virus stays localized to one site, which for HSV-2 is usually the genital region. Mice, in contrast, would never normally contract either human herpes variant, so their bodies react very differently to it. HSV-2 is a traditionally human pathogen: Although there is some debate around how and when HSV-2 made the jump to humans, Koelle says it has been coevolving with us for at least 1 million years. University of Washington translational immunologist David Koelle, who didn’t work on the study, agrees this is a fascinating study, but is “not sure how relevant is to humans,” because HSV-2 interacts with the mouse body differently than it does humans. “It was a surprise that they found obesity actually played into viral infections in more of a positive fashion,” says Lorne Kastrukoff, a University of British Columbia neurologist who has studied herpes in the past but didn’t participate in the new study. The study authors did not respond to The Scientist’s requests for comment. Based on this information, the scientists posit in their paper that obesity causes more gut-derived bacteria to move into the genital tract, and that these microbes mitigate HSV-2’s lethal effects by controlling the levels of γδ T-cells and other immune cells. coli into the vaginal microbiomes of lean mice, they found that it promoted viral clearance and prevented HSV-2 symptoms compared to controls. The microbiota of obese mice differed from that of the lean mice, with a higher level of gut-derived bacteria such as E. Performing a similar analysis on the greater vaginal microbiome, the team found that administering antibiotics to remove commensal vaginal microbiota also significantly decreased obese mice’s survival. The obese mice also started clearing the virus from their genital mucosa sooner. To their surprise, they found that while all the lean mice died in the first two weeks, half of the obese mice survived the three-week period. The KAIST scientists write in the study that they expected it to increase susceptibility to HSV-2. ![]() They then intravaginally infected all of the mice with HSV-2 virus and observed their immune response over the course of three weeks. The researchers gave some of the mice standard food and fed others a high-fat diet. In comparing the immune response of lean and obese female mice, the study authors write in the study that they hoped to find out how obesity affects the immune response of the genital mucosa. Genital herpes affects more than 11 percent of people between the ages of 15 and 49, but has no cure. HSV-2 originated later in human history than the more prevalent HSV-1 type, which is known for causing oral herpes. Researchers at the Korea Advanced Institute of Science and Technology (KAIST) led by immunologist Heung Kyu Lee wanted to test obesity’s effects on antiviral immunity, specifically against the common human sexually transmitted infection genital herpes. Although obesity has been linked to a higher risk of cervical cancer mortality in women, scientists haven’t found any evidence of a link between herpes and obesity, according to the study. The finding offers insight into the mechanisms behind vaginal immune responses and the role of the microbiome in combating disease.īiomedical scientists have linked obesity in humans to higher risk of cardiovascular disease, as well as greater cancer risk and in some cases impaired immune systems. In a study published November 8 in Cell Reports, researchers found that thanks to differences in their vaginal microbiomes compared with lean mice, obese mice fed a high-fat diet had stronger immune responses against HSV-2, which causes genital herpes in humans. Injecting mice with human pathogens such as herpes simplex virus (HSV), as is often done in lab studies, can kill them in a matter of days. For a human, herpes is usually no more than a painful inconvenience, but for a mouse, catching the sexually transmitted infection is akin to a kiss of death.
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