Measles virus (Morbillivirus abbreviated as MV, but more recently MeV) is the causal agent of measles disease, thought to have existed at least 4,000 years ago, affecting predominantly infants, but also immunocompromised individuals remaining a public health issue today globally. In this review, we discuss the historical background about MeV infection to modern-day research on measles disease, current epidemiology, but also what is known about immunisation against it. We report what is known about the viral structure and the function of the viral proteins. This additionally covers the cellular structure of MeV, mechanisms, and clinical aspects of infection. Including a review of topics like cellular receptor-associated entry factors, to the immunology of MeV infection. In this review, the current knowledge of innate immune responses during infection is explained, which involves changes to chemokine and cytokine expression, finalised by the present understanding of adaptive immune responses to MeV. The genomic stability of the MeV proteins is explained and suggestive that it could be the third pathogen with eradication potential (after the variola and rinderpest viruses). Further biological and immunological clarification as to how this could occur is explained below.

The narrative review aims to shed light on the influence of inflammation in the comorbid chronic pain and major depressive disorder (MDD). This connection is known to be multifactorial, with a dynamic interaction between genetic and epigenetic factors. However, a growing body of evidence has shown that the co-presence of MDD and pain is underlain by immune mechanisms involved in the persistence of the inflammatory process. In particular, the cytokines released following activation of the innate immune system during inflammation cause changes at the endocrine level that result in glucocorticoid resistance, as well as altering the synthesis and metabolism of some central nervous system (CNS) mediators. Cytokines appear to generate neuroinflammation by activating normally protective microglia. Various other mechanisms, including changes in the function of the glutamatergic, GABAergic, and serotonergic systems are also implicated, but inflammation-induced reduction of BDNF (brain-derived neurotrophic factor) appears to be the deciding factor. In turn, neuroinflammation leads to sickness behavior, which is characterized by anhedonia and social withdrawal. This review explored these mechanisms, which may be at the root of comorbid pain and MDD. Although intriguing, however, most available evidence comes from animal studies, and rigorous clinical exploration is warranted.