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Thrombocytopenia, or a low platelet count of less than 150 × 109/L, is a typical observation in the outcome or during numerous viral infections.
Thrombocytopenia, or a low platelet count of less than 150 × 109/L, is a typical observation in the outcome or during numerous viral infections. Mild thrombocytopenia mixed with lymphopenia in a patient with signs and symptoms of an infectious disease enhances the possibility of a viral infection in clinical medicine. Platelet consumption owing to inflammation-induced coagulation, sequester from the circulation by phagocytosis and hypersplenism, and decreased platelet generation due to faulty megakaryopoiesis or cytokine-induced myelosuppression are all traditional explanations for this occurrence. Virus-induced thrombocytopenia, except for viral hemorrhagic fevers and rare cases of severe disseminated viral infections, does not cause major bleeding, requires few platelet transfusions, and is thus readily ignored as clinically irrelevant. Important findings emerge when the link between platelets and viral infection is explored more closely and in bigger study groups, shedding light on previously unknown features of viral illnesses. Individuals with influenza virus infection have a higher risk of thromboembolic consequences during and after illness.
Herein, platelets are small, anucleate cells that circulate in the blood for roughly 7 to 10 days after they are created. Their principal physiological function is hemostasis, which involves the formation of blood clots (thrombi) to protect vascular integrity. Megakaryocytes, which are gigantic polyploid cells that reside in the bone marrow and are generated from hematopoietic stem cells, are the source of platelets. After endoplasmic maturation, megakaryocytes produce proplatelets, which bud out many platelets into the bloodstream. Platelets circulate at levels of 150 to 450 × 109/L in people with normal bone marrow function.
Platelet interaction and response to the virus
The virus infects a susceptible cell by attaching to a surface receptor, which then mediates its internalization via the endocytic route. The capacity of the virus to avoid endosomal acidification and lysosomal fusion through several pathways, delivering its genome to the cytoplasm or nucleus depending on the viral type, is essential for successful infection. The host cell has evolved mechanisms for recognizing and combating viral infection at each stage of viral replication, mostly by triggering the production of antiviral restriction factors in bystander cells via type I IFN signaling. Platelets have been found to have surface receptors capable of mediating viral binding and entry.
Platelet activation in Dengue
Thrombocytopenia is a common symptom of dengue fever, and a reduction in platelet counts corresponds to hemodynamic instability and severity progression, while its recovery corresponds to clinical improvement and hospital release. The pathophysiologic mechanisms causing severe dengue fever patients are unknown. DENV pathology and severity are thought to be favoured by immune activation with higher levels of cytokines and other pro-inflammatory mediators that target the vascular endothelium. This mechanism has been demonstrated to involve the activation of immune cells such as B and T cells, monocytes, macrophages, and dendritic cells. Dengue patients have been shown to have higher platelet activation, which has been linked to the severity of the disease. P-select in and CD63 expression (translocated from and dense-granules, respectively), phosphatidylserine exposure, and inside-out activation of IIb3 integrin are all surface markers of activation that correspond with platelet count drop during dengue infection. Platelet stimulation may contribute to platelet loss by inducing platelet deposition in the peripheral micro vascular bed. Platelet aggregation and fibrinogen deposition have both been found in postmortem histology micro vessels and skin biopsies from severe dengue infections. Increased platelet apoptosis, in addition to platelet activation and intravascular thrombosis, may contribute to thrombocytopenia in dengue infection. Thrombocytopenia in dengue may be caused by central processes of bone marrow suppression, in addition to platelet death and aggregation at the periphery. DENV propagation in bone marrow may cause hematopoiesis inhibition in all lineages, including megakaryocytic lineages. Dengue patients’ bone marrow aspirates demonstrate considerable hypocellularity and a halt in granulocyte, megakaryocyte, and erythroid/myeloid precursor maturation.
Platelet activation in influenza virus
Influenza pneumonia, caused by virulent strains of influenza A virus (IAV), remains a major global health problem with seasonal influenza epidemics and unexpected pandemics that have occurred for more than a century. the virulent H1N1 strain of influenza identified in the 2009 flu pandemic caused increased morbidity and mortality worldwide. Patients admitted in intensive care unit (ICU) with severe influenza pneumonia usually presented acute lung injury and acute respiratory distress syndrome (ALI/ARDS) which have exacerbated immune response and increased systemic and airway inflammation as central features of pathogenesis. Increased platelet activation and platelet–monocyte aggregation after influenza vaccination correlated with the expansion of inflammatory CD14highCD16+ and reduction of classical CD14highCD16− monocyte subsets, which was prevented by antiplatelet therapy with aspirin or clopidogrel. Histopathological studies of lungs in experimental influenza A infection in mice and autopsies from patients who expired from H1N1 influenza documented frequent micro vascular thrombosis in areas of disrupted integrity of alveolar-capillary barrier. In influenza A-infected mice, platelet infiltration to lung parenchyma was evidenced by CD41 and PF4 immunohistochemistry, transmission electron microscopy, and platelet counting in bronchoalveolar lavage (BAL). Ultra structural analysis of infiltrated platelets shows evidence of platelet activation and formation of platelet–neutrophil aggregates, which are in agreement with increased levels of serotonin, sP-selectin, and sCD40L in bronchoalveolar lavage.
Platelets are dynamic cells that participate in inflammation and prothrombotic reactions in a variety of vascular and inflammatory events, including viral infections, according to new data. Platelets have developed new activities over time, and they are increasingly being recognized as immune cells. Platelet reactions have been implicated in the pathophysiology of dengue fever, influenza pneumonia and other viral infections i.e., HIV.
Dr. Supriya Jaiswal
Chief Consultant, S M Hospital, Patna, Bihar. Secretary, Patna Obs & Gyn Society. East Zone Coordinator, Adolescent Health Committee, FOGSI.