Host–Virus Immune Interactions in Andes Virus Infection: Implications for Human-to-Human Transmission, Pathogenesis, and Public Health

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Abstract
The Andes virus (ANDV, Orthohantavirus, andesense) is unique among hantaviruses in that it may transfer from person to person and cause severe vascular damage. The evidence on host–virus immunological interactions and their importance in disease progression, transmission, and public health is compiled in this narrative review. ANDV mostly affects pulmonary endothelial cells and does not result in widespread cell loss. Rather, the loss of vascular barrier integrity is caused by vascular endothelial growth factor (VEGF) signaling, Ras homolog family member A (RhoA) activation, breakdown of vascular endothelial (VE)-cadherin, hypoxia-related pathways, and mediators produced from infected pericytes. Additionally, the virus interferes with early antiviral defenses involving protein kinase R (PKR), TANK-binding kinase 1 (TBK1)–interferon regulatory factor 3 (IRF3), mitochondrial antiviral-signaling protein (MAVS), and retinoic acid-inducible gene I (RIG-I)/melanoma differentiation-associated protein 5 (MDA5). The intensity or outcome of the disease has been associated with increased interleukin-6 (IL-6), altered complement activity, thrombocytopenia, neutralizing-antibody reactions, and specific host genetic variations; nevertheless, significant T-cell activation does not necessarily correspond with viral clearance. Blood and a number of mucosal and secretory samples have been found to contain ANDV ribonucleic acid (RNA), albeit RNA discovery by itself does not prove the presence of an infectious virus. Epidemiological evidence indicates that Secondary transmission is rare and mostly linked to extended close or intimate contact. Genomic sequencing, when paired with epidemiological evidence, can shed light on transmission chains. Recent outbreaks linked to travel further emphasize the significance of worldwide surveillance and coordinated contact tracing. Prospective studies integrating genomic analysis, serial virological sampling, and standardized exposure evaluation are required to more effectively define the infectious phase and transmission patterns

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