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ANDV
ANDV Full Name
Andes Virus
ANDV Introduction
Andes virus (ANDV) is a New World hantavirus within the family Hantaviridae, order Bunyavirales, and is the principal etiological agent of hantavirus pulmonary syndrome (HPS) in South America. First identified in 1995 during an outbreak in Patagonia, Argentina, ANDV is carried by the long-tailed colilargo mouse (Oligoryzomys longicaudatus) as its natural reservoir. The virus possesses a tri-segmented, single-stranded, negative-sense RNA genome comprising the large (L), medium (M), and small (S) segments, which encode the RNA-dependent RNA polymerase (RdRp), the glycoprotein precursor (yielding Gn and Gc), and the nucleocapsid protein (NP), respectively. ANDV is phylogenetically classified within the genus Orthohantavirus and is most closely related to other South American hantaviruses such as Oran virus and Lechiguanas virus. ANDV is distinguished as the only hantavirus definitively demonstrated to support person-to-person transmission, a feature of major public health significance that sets it apart from all other known hantaviruses.
Figure 1. Andes Virus Genome Mutations That Are Likely Associated with Animal Model Attenuation and Human Person-to-Person Transmission.
ANDV targets vascular endothelial cells, particularly those lining the pulmonary microvasculature, leading to increased capillary permeability, pulmonary edema, and the life-threatening respiratory compromise characteristic of HPS. The virus enters host cells through β3 integrin-mediated endocytosis, exploiting the expression of αvβ3 integrin on endothelial cells and platelets. Following entry, ANDV replicates in the cytoplasm and assembles new virions that bud into the Golgi apparatus. The NP plays a central role in viral RNA encapsidation, polymerase recruitment, and immune evasion through inhibition of interferon responses. ANDV infection triggers a dysregulated innate immune response characterized by elevated levels of TNF-α, IL-6, and other proinflammatory cytokines, contributing to the cytokine storm implicated in HPS pathogenesis. The virus also interferes with complement activation and endothelial barrier integrity through Gn-mediated signaling pathways. Cellular immune responses, particularly CD8+ T cell activity directed against NP and glycoprotein epitopes, are critical for viral clearance, while neutralizing antibodies against Gn/Gc develop during convalescence.
ANDV causes a severe form of HPS with case fatality rates approaching 30–40%, significantly higher than many other hantavirus infections. The disease is characterized by a prodromal febrile phase followed by rapid progression to cardiopulmonary failure. Diagnosis relies on serological detection of IgM and IgG antibodies against ANDV NP and glycoproteins by ELISA, confirmed by reverse transcription-polymerase chain reaction (RT-PCR) targeting the S and M segments. There is currently no FDA-approved antiviral therapy or vaccine for ANDV infection, and clinical management remains supportive, often requiring mechanical ventilation and extracorporeal membrane oxygenation (ECMO). Ribavirin has shown limited efficacy in HPS treatment. Several vaccine platforms are under investigation, including recombinant adenovirus vectors, DNA vaccines, and virus-like particle (VLP) formulations expressing ANDV antigens. The capacity of ANDV for person-to-person spread underscores the importance of developing effective post-exposure prophylaxis. Monoclonal antibody-based therapeutics targeting the glycoprotein complex represent a promising avenue for intervention, with several candidates demonstrating protection in preclinical hamster models.
Alternate Names for ANDV
Andes Virus; ANDV; ANDV Spike; ANDV S Protein; Hantavirus
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