Subject(s)
Central Nervous System/virology , Forkhead Transcription Factors/immunology , SARS-CoV-2/physiology , T-Lymphocytes, Regulatory/immunology , Animals , CD4 Antigens/immunology , COVID-19/complications , COVID-19/immunology , COVID-19/virology , Central Nervous System/immunology , Central Nervous System Diseases/complications , Central Nervous System Diseases/immunology , Central Nervous System Diseases/virology , Humans , Interleukin-2 Receptor alpha Subunit/immunology , Neuropilin-1/immunology , SARS-CoV-2/immunologyABSTRACT
Burkholderia pseudomallei (B. pseudomallei) causes melioidosis, a potentially fatal disease for which no licensed vaccine is available thus far. The host-pathogen interactions in B. pseudomallei infection largely remain the tip of the iceberg. The pathological manifestations are protean ranging from acute to chronic involving one or more visceral organs leading to septic shock, especially in individuals with underlying conditions similar to COVID-19. Pathogenesis is attributed to the intracellular ability of the bacterium to 'step into' the host cell's cytoplasm from the endocytotic vacuole, where it appears to polymerize actin filaments to spread across cells in the closer vicinity. B. pseudomallei effectively evades the host's surveillance armory to remain latent for prolonged duration also causing relapses despite antimicrobial therapy. Therefore, eradication of intracellular B. pseudomallei is highly dependent on robust cellular immune responses. However, it remains ambiguous why certain individuals in endemic areas experience asymptomatic seroconversion, whereas others succumb to sepsis-associated sequelae. Here, we propose key insights on how the host's surveillance radars get commandeered by B. pseudomallei.
Subject(s)
Burkholderia pseudomallei/immunology , Immunologic Surveillance , Melioidosis/immunology , Animals , Burkholderia pseudomallei/pathogenicity , Host Microbial Interactions , Humans , VirulenceABSTRACT
A vast proportion of coronavirus disease 2019 (COVID-19) individuals remain asymptomatic and can shed severe acute respiratory syndrome (SARS-CoV) type 2 virus to transmit the infection, which also explains the exponential increase in the number of COVID-19 cases globally. Furthermore, the rate of recovery from clinical COVID-19 in certain pockets of the globe is surprisingly high. Based on published reports and available literature, here, we speculated a few immunovirological mechanisms as to why a vast majority of individuals remain asymptomatic similar to exotic animal (bats and pangolins) reservoirs that remain refractile to disease development despite carrying a huge load of diverse insidious viral species, and whether such evolutionary advantage would unveil therapeutic strategies against COVID-19 infection in humans. Understanding the unique mechanisms that exotic animal species employ to achieve viral control, as well as inflammatory regulation, appears to hold key clues to the development of therapeutic versatility against COVID-19.