Infection with the most common member of the herpesvirus family, HHV-6, significantly accelerated the development and progression of a multiple sclerosis-like disease in monkeys, a new study reports.
The study, "Herpesvirus trigger accelerates neuroinflammation in a nonhuman primate model of multiple sclerosis". was published in the journal Proceedings of the National Academy of Sciences of the United States of America (PNAS). It further supports the theory that viral infections play a role in triggering conditions like MS.
In the study researchers gave a group of marmoset monkeys doses of human herpesvirus 6 (HHV-6) for four months. They then checked whether the animals mounted an immune response against the virus, and found those given the HHV-6 virus were positive for antibodies against it, while a group of control animals (those not given the HHV-6 virus) were negative.
Next, researchers induced experimental autoimmune encephalomyelitis (EAE) in both infected and control animals, and monitored them frequently for signs of disease. Marmosets given HHV-6 developed symptoms around day 80 after EAE induction, while control animals showed no symptoms at day 200.
Experimental autoimmune encephalomyelitis marmosets infected with HHV-6 also died in a significantly shorter period following EAE induction compared to control animals. Brain scans using magnetic resonance imaging (MRI), showed a trend for HHV-6-infected animals to develop lesions earlier.
At the study’s end researchers analysed samples of the monkeys’ central nervous system (CNS, brain and spinal cord). Once again they detected signs of HHV-6 in the virus-infected animals in several locations within the CNS. In the brain of a subgroup of animals infected with HHV-6 but without induced EAE, evidence of the virus was rare.
Finally, researchers found greater numbers of pro-inflammatory immune cells called CD8 T-cells — cells that secrete a pro-inflammatory signalling molecule called interferon gamma — in the EAE marmosets infected with HHV-6.
“Our data support the hypothesis that viruses may act as triggers to lower the threshold for autoimmunity, and warrant trials of antiviral interventions in early disease stages,” the researchers wrote.
Source: MS-UK 29/10/2018