Interplay between activation of endogenous retroviruses and inflammation as common pathogenic mechanism in neurological and psychiatric disorders.

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There is a bit weird observation about drugs that had a successful phase II in ALS: On third of those drugs can counter HIV.

Human Endogenous retroviruses (ERVs) are elements in the genome that closely resemble retroviruses. They comprise up to 5–8% of the human genome. They have repeatedly been implicated in the aetiology and pathophysiology of numerous human disorders, particularly in those that affect the central nervous system.

There is evidence that HERVs can be reactivated by viral infections, such as: 1) retroviruses – human immunodeficiency virus type-1 (HIV-1), human T-lymphotropic virus 1 (HTLV-1);

2) RNA viruses – influenza A virus, hepatitis C virus (HCV), severe acute respiratory syndrome coronavirus-2 (SARSCoV-2);

3) DNA viruses – herpes simplex virus type-1 (HSV-1), Epstein-Barr virus (EBV), human cytomegalovirus (CMV), Kaposi’s sarcoma-associated herpesvirus (KSHV) [66]

A growing number of studies links the induction and expression of these retroviral elements with the onset and severity of neurodevelopmental and psychiatric disorders.

Although these disorders differ in terms of overall disease pathology and causalities, a certain degree of chronic inflammation can be identified in all of them.

Based on these commonalities, the authors discuss in this new publication of the bidirectional relationship between ERV expression and inflammation and highlight that numerous entry points to this reciprocal sequence of events exist, including initial infections with ERV-activating pathogens, exposure to non-infectious inflammatory stimuli, and conditions in which epigenetic silencing of ERV elements are disrupted.

Read the original article on Pubmed

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