B — Bunyaviruses (Order Bunyavirales)
Bunyaviruses comprise a large and diverse group of enveloped, negative-sense single-stranded RNA viruses within the order Bunyavirales. Their genomes are typically tripartite, consisting of small (S), medium (M), and large (L) segments encoding the nucleoprotein (N), glycoproteins (Gn and Gc), and RNA-dependent RNA polymerase (L), respectively. Replication occurs in the cytoplasm, and viral assembly takes place at the Golgi apparatus — a distinguishing feature among RNA viruses.
Many bunyaviruses are arboviruses, transmitted by mosquitoes, ticks, or sandflies, while others are rodent-borne. Several families within the order are medically important, including Hantaviridae, Nairoviridae, and Phenuiviridae.
Hantaviruses (e.g., Sin Nombre virus, Hantaan virus) are transmitted via inhalation of aerosolized rodent excreta and cause either hantavirus pulmonary syndrome (HPS) or hemorrhagic fever with renal syndrome (HFRS). A hallmark of hantavirus pathogenesis is noncytopathic infection of endothelial cells, with disease driven largely by immune-mediated capillary leak and cytokine dysregulation rather than direct viral destruction. HPS is characterized by rapid-onset pulmonary oedema and cardiogenic shock, reflecting capillary leakage in the lungs.
Humans are incidental hosts. After inhalation, hantaviruses infect endothelial cells via β3 integrins. Unlike many lytic viruses, hantaviruses do not cause direct endothelial destruction. Instead, disease results largely from immune-mediated capillary leak. Infected endothelial cells increase vascular permeability in response to proinflammatory cytokines.
Crimean-Congo hemorrhagic fever virus (CCHFV), a tick-borne nairovirus, causes severe hemorrhagic disease with high mortality. Viral proteins antagonize interferon responses, enabling high viremia. Endothelial dysfunction, coagulopathy, and dysregulated inflammatory responses contribute to shock and multiorgan failure.
Rift Valley fever virus (RVFV), transmitted by mosquitoes, infects hepatocytes and macrophages. Severe disease includes hepatitis, retinitis, and occasionally hemorrhagic fever or encephalitis. The viral NSs protein potently suppresses host transcription and interferon signaling, enhancing virulence.
Across bunyaviruses, innate immune evasion, vascular permeability, and immunopathology are central themes. Research focuses on viral polymerase function, interferon antagonists, zoonotic spillover, and vaccine development. Their segmented genomes also allow reassortment, facilitating emergence of novel pathogenic strains.
Bunyaviruses comprise a large and diverse group of enveloped, negative-sense single-stranded RNA viruses within the order Bunyavirales. Their genomes are typically tripartite, consisting of small (S), medium (M), and large (L) segments encoding the nucleoprotein (N), glycoproteins (Gn and Gc), and RNA-dependent RNA polymerase (L), respectively. Replication occurs in the cytoplasm, and viral assembly takes place at the Golgi apparatus — a distinguishing feature among RNA viruses.
Many bunyaviruses are arboviruses, transmitted by mosquitoes, ticks, or sandflies, while others are rodent-borne. Several families within the order are medically important, including Hantaviridae, Nairoviridae, and Phenuiviridae.
Hantaviruses (e.g., Sin Nombre virus, Hantaan virus) are transmitted via inhalation of aerosolized rodent excreta and cause either hantavirus pulmonary syndrome (HPS) or hemorrhagic fever with renal syndrome (HFRS). A hallmark of hantavirus pathogenesis is noncytopathic infection of endothelial cells, with disease driven largely by immune-mediated capillary leak and cytokine dysregulation rather than direct viral destruction. HPS is characterized by rapid-onset pulmonary oedema and cardiogenic shock, reflecting capillary leakage in the lungs.
Humans are incidental hosts. After inhalation, hantaviruses infect endothelial cells via β3 integrins. Unlike many lytic viruses, hantaviruses do not cause direct endothelial destruction. Instead, disease results largely from immune-mediated capillary leak. Infected endothelial cells increase vascular permeability in response to proinflammatory cytokines.
Crimean-Congo hemorrhagic fever virus (CCHFV), a tick-borne nairovirus, causes severe hemorrhagic disease with high mortality. Viral proteins antagonize interferon responses, enabling high viremia. Endothelial dysfunction, coagulopathy, and dysregulated inflammatory responses contribute to shock and multiorgan failure.
Rift Valley fever virus (RVFV), transmitted by mosquitoes, infects hepatocytes and macrophages. Severe disease includes hepatitis, retinitis, and occasionally hemorrhagic fever or encephalitis. The viral NSs protein potently suppresses host transcription and interferon signaling, enhancing virulence.
Across bunyaviruses, innate immune evasion, vascular permeability, and immunopathology are central themes. Research focuses on viral polymerase function, interferon antagonists, zoonotic spillover, and vaccine development. Their segmented genomes also allow reassortment, facilitating emergence of novel pathogenic strains.