[13] Investigations of the subcellular localization of the MERS-CoV M protein found C-terminal sequence signals associated with trafficking to the Golgi.

[5] Studies of the SARS-CoV M protein suggest that M-M interactions involve both the N- and C-termini.

[4] Incorporation of the spike protein (S) - which is required for assembly of infectious virions - is reported to occur though M interactions and may depend on specific conformations of M.[5][13] The conserved amphipathic region C-terminal to the third transmembrane segment is important for spike interactions.

[13] Interactions with M appear to be required for correct subcellular localization of S at the viral budding site.

[16] Antibodies to epitopes found in the M protein have been identified in patients recovered from severe acute respiratory syndrome (SARS).

[18] Other recent research has identified that SAS-COV-2 membrane protein when treated on human PBMC's causes a significant increase in pro inflammatory mediators such as TNF and IL-6.

In these studies, exogenous membrane protein treated intra nasally caused a significant increase in pulmonary inflammation in mice leading to histological changes within the lungs.

[21] A study of SARS-CoV-2 sequences collected during the COVID-19 pandemic found that missense mutations in the M gene were relatively uncommon and suggested it was under purifying selection.

[22] Similar results have been described for broader population genetics analyses over a wider range of related viruses, finding that the sequences of M and several non-structural proteins in the coronavirus genome are most subject to evolutionary constraints.