Platelets, best known as essential effector cells in coagulation and hemostasis, are increasingly recognized as major inflammatory cells that play a role in the innate and adaptive arms of the immune system. The interaction of platelets with various cell types of the innate immune system, particularly neutrophils as well as with structural cells of the vascular endothelium, induces the release of platelet-derived mediators, thus exerting a protective effect in the physiologic response to diseases. However, platelet-driven activation of neutrophils and endothelium, if excessive and poorly controlled, may result in thrombo-inflammatory events which could predispose to the development of organ damage and dysfunction. This aspect is particularly relevant in the context of acute and chronic manifestations and complications of infectious diseases.
Notably, while much work has been done to explore the role of platelets in the development of chronic cardiovascular diseases, little is known about their contribution to the pathophysiology of the acute and chronic manifestations of infectious diseases. The human immunodeficiency virus (HIV), Mycobacterium tuberculosis (TB) and Streptococcus pneumoniae (pneumococcus) are some of the most prevalent and deadly infectious diseases globally. Lower respiratory infections, of which pneumococcus is the most common cause, and TB are among the top 10 causes of death, while ~38 million people are currently living with HIV. Platelets are hypothesized to contribute not only to the acute clinical manifestations of these diseases, but also to the chronic, long-term complications. For instance, platelets are proposed to drive a proinflammatory, tissue-degrading phenotype in TB, as well as being a major contributor to the cardiovascular mortality related to pneumonia. In the context of HIV, where morbidity and mortality from non-AIDS-related conditions, such as cardiovascular and neurocognitive disease, have overtaken those caused by opportunistic infections, the role of chronic platelet activation induced by the virus and/or its treatment remains relatively unexplored.
In this Research Topic, we welcome the submission of Original Research, Review and Mini-Review articles that cover different aspects of the role of platelet activation in the acute and chronic manifestations of HIV, TB and pneumococcal disease. We specifically encourage studies that cover, but are not limited to, to the following topics:
1. The role of platelet activation in the development of acute cardiovascular complications in HIV, TB or pneumococcus infection.
2. The role of platelet activation in the pathogenesis of chronic manifestations and/or complications of HIV, TB or the pneumococcus infection.
3. The effect of anti-infective treatment for HIV, TB and pneumococcal disease on platelet activation and function.
4. New therapeutic strategies targeting platelet activation in the setting of HIV, TB and the pneumococcus infection.
Platelets, best known as essential effector cells in coagulation and hemostasis, are increasingly recognized as major inflammatory cells that play a role in the innate and adaptive arms of the immune system. The interaction of platelets with various cell types of the innate immune system, particularly neutrophils as well as with structural cells of the vascular endothelium, induces the release of platelet-derived mediators, thus exerting a protective effect in the physiologic response to diseases. However, platelet-driven activation of neutrophils and endothelium, if excessive and poorly controlled, may result in thrombo-inflammatory events which could predispose to the development of organ damage and dysfunction. This aspect is particularly relevant in the context of acute and chronic manifestations and complications of infectious diseases.
Notably, while much work has been done to explore the role of platelets in the development of chronic cardiovascular diseases, little is known about their contribution to the pathophysiology of the acute and chronic manifestations of infectious diseases. The human immunodeficiency virus (HIV), Mycobacterium tuberculosis (TB) and Streptococcus pneumoniae (pneumococcus) are some of the most prevalent and deadly infectious diseases globally. Lower respiratory infections, of which pneumococcus is the most common cause, and TB are among the top 10 causes of death, while ~38 million people are currently living with HIV. Platelets are hypothesized to contribute not only to the acute clinical manifestations of these diseases, but also to the chronic, long-term complications. For instance, platelets are proposed to drive a proinflammatory, tissue-degrading phenotype in TB, as well as being a major contributor to the cardiovascular mortality related to pneumonia. In the context of HIV, where morbidity and mortality from non-AIDS-related conditions, such as cardiovascular and neurocognitive disease, have overtaken those caused by opportunistic infections, the role of chronic platelet activation induced by the virus and/or its treatment remains relatively unexplored.
In this Research Topic, we welcome the submission of Original Research, Review and Mini-Review articles that cover different aspects of the role of platelet activation in the acute and chronic manifestations of HIV, TB and pneumococcal disease. We specifically encourage studies that cover, but are not limited to, to the following topics:
1. The role of platelet activation in the development of acute cardiovascular complications in HIV, TB or pneumococcus infection.
2. The role of platelet activation in the pathogenesis of chronic manifestations and/or complications of HIV, TB or the pneumococcus infection.
3. The effect of anti-infective treatment for HIV, TB and pneumococcal disease on platelet activation and function.
4. New therapeutic strategies targeting platelet activation in the setting of HIV, TB and the pneumococcus infection.
