DescriptionAround 95% of humans are exposed to human herpesvirus-6 and -7 (HHV-6, HHV-7) during early childhood. After the primary infection viruses can establish life-long persistency without visible clinical changes, however the factors reactivating viral infection from latency and role of these beta-herpesviruses in the development of non-communicable diseases are not completely clarified.
Several reports based on epidemiological, immunological, molecular biological and morphological evidences support the hypothesis that HHV-6A/B and HHV-7 could be potential triggers of autoimmune diseases development, such as rheumatoid arthritis, autoimmune thyroiditis as well as diseases associated with nervous system - fibromyalgia, encephalopathy and myalgic encephalomyelitis/chronic fatigue syndrome. Two well-explored explanations for autoimmunity after viral infection are molecular mimicry and the bystander effect. In molecular mimicry, similarities between a viral protein and a cellular protein result in immune cells mistakenly attacking the body, while in the bystander effect, the high level of inflammation induced by viral infection activates immune cells and leads them to attack healthy tissue.
In a similar manner to mentioned human beta-herpesviruses also SARS-CoV-2 may have the ability to contribute to autoimmunity. Numerous records demonstrate the likelihood of COVID-19 patients to develop over 15 separate types of autoantibodies along with above 10 distinct autoimmune diseases.
|Period||10 Jun 2022|
|Event title||8th National Conference with International Participation "Morphological Days"|
|Organiser||Institute of Experimental Morphology, Pathology and Anthropology, Bulgarian Academy of Sciences|
|Degree of Recognition||International|