The loss of immune memory against previously encountered pathogens, which has been reported in measles virus (MV)-infected humans and macaques, provides further support to the crucial need for measles vaccination on a global scale. Indeed, this newly characterized immunomodulatory process sums itself to the well-known viral immunosuppressive effects, thereby representing an additional explanatory key for the >100,000 deaths annually caused by MV. Within such framework, it would be of interest to know the role, if any, played by viral-specific and host-specific factors in the development of MV-induced "immunological amnesia" (IA). More in detail, to what extent does IA depend upon the viral strain responsible for the infection? And, are there any differences, in terms of IA magnitude, between Th1-dominant versus Th2-dominant individuals infected by MV? We are investigating since many years wild dolphins naturally infected with cetacean morbillivirus (CMV), a devastating pathogen closely related to MV. These animals frequently develop an immunosuppression similar to that experienced by MV-infected humans, although Guiana dolphins (Sotalia guianensis) harboring a given CMV strain may undergo an even more prominent, multicentric lymphoid cell depletion. These viral strain-driven differences in the severity of host's immunodeficiency could be accompanied, among others, by different expression levels of the SLAM/CD150 immune cell viral receptor - specifying the well-documented lymphotropism of both animal and human morbilliviruses - in Th1-dominant as compared to Th2-dominant individuals. Similar viral-host interaction dynamics could also modulate MV-induced IA, although we don't know if CMV-infected dolphins may develop any IA-like condition. Comparative immunopathological and immunopathogenetic studies in CMV-infected cetaceans may thus provide valuable insight into a more in-depth understanding of MV-induced IA, thereby setting a parallel infection model for an ad hoc dissection of virus-related and host-related factors involved in the determinism of this alarming condition.
Measles, immune amnesia, and cetaceans
Di Guardo G
;
2019-01-01
Abstract
The loss of immune memory against previously encountered pathogens, which has been reported in measles virus (MV)-infected humans and macaques, provides further support to the crucial need for measles vaccination on a global scale. Indeed, this newly characterized immunomodulatory process sums itself to the well-known viral immunosuppressive effects, thereby representing an additional explanatory key for the >100,000 deaths annually caused by MV. Within such framework, it would be of interest to know the role, if any, played by viral-specific and host-specific factors in the development of MV-induced "immunological amnesia" (IA). More in detail, to what extent does IA depend upon the viral strain responsible for the infection? And, are there any differences, in terms of IA magnitude, between Th1-dominant versus Th2-dominant individuals infected by MV? We are investigating since many years wild dolphins naturally infected with cetacean morbillivirus (CMV), a devastating pathogen closely related to MV. These animals frequently develop an immunosuppression similar to that experienced by MV-infected humans, although Guiana dolphins (Sotalia guianensis) harboring a given CMV strain may undergo an even more prominent, multicentric lymphoid cell depletion. These viral strain-driven differences in the severity of host's immunodeficiency could be accompanied, among others, by different expression levels of the SLAM/CD150 immune cell viral receptor - specifying the well-documented lymphotropism of both animal and human morbilliviruses - in Th1-dominant as compared to Th2-dominant individuals. Similar viral-host interaction dynamics could also modulate MV-induced IA, although we don't know if CMV-infected dolphins may develop any IA-like condition. Comparative immunopathological and immunopathogenetic studies in CMV-infected cetaceans may thus provide valuable insight into a more in-depth understanding of MV-induced IA, thereby setting a parallel infection model for an ad hoc dissection of virus-related and host-related factors involved in the determinism of this alarming condition.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
