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Mayaro virus (MAYV) is a mosquito-borne alphavirus (family Togaviridae) endemic to tropical forests of Central and South America. It is the causative agent of Mayaro fever, a debilitating acute illness often confused with dengue or chikungunya, characterized by high fever, rash, and severe, prolonged polyarthralgia. While historically considered a sporadic rural disease, recent evidence suggests MAYV is adapting to urban transmission cycles, involving new mosquito vectors like Aedes aegypti, raising significant concerns for potential widespread epidemics. There are no licensed vaccines or specific antiviral therapies.
The MAYV virion is spherical, ~70 nm in diameter, with an icosahedral nucleocapsid core surrounded by a host-derived lipid bilayer.
Figure 1. (A) Structure of MAYV. (B) Schematic representation of the MAYV genome. (Wei L L L,et al, 2024)
MAYV belongs to the genus Alphavirus within the family Togaviridae. It is a member of the Semliki Forest antigenic complex, which also includes chikungunya (CHIKV), Ross River, and O'nyong-nyong viruses. Genetic analyses distinguish three major genotypes: L (widely distributed in Brazil, Peru, Bolivia, and Trinidad), D (found in Haiti and Brazil), and N (limited to Peru). Recent strains show evolutionary signatures of adaptation to urban mosquito vectors, including mutations in the E2 envelope protein that enhance infectivity for Aedes species.
MAYV entry into host cells is initiated by the binding of the viral envelope glycoprotein E2 to specific cell surface receptors, followed by endocytosis and fusion of the viral envelope with the endosomal membrane, releasing the viral genome into the cytoplasm. This process is dependent on the conformational changes of E1 and E2 glycoproteins triggered by the acidic environment of the endosome. Key viral and host factors involved in this step include the E2 glycoprotein (which mediates receptor binding) and host cell receptors such as Mxra8 and ApoER2, as well as potential additional receptors like VLDLR. Mutations in the E2 glycoprotein, such as E2-T179N and E2-Q183P, have been shown to alter viral tropism, enhancing replication in mosquito cells while reducing dependence on human receptors like Mxra8 and ApoER2.
MAYV exhibits tropism for a variety of host cell types, including fibroblasts, endothelial cells, monocytes, macrophages, and chondrocytes (joint cells), which explains the clinical manifestations of Mayaro fever. Infection of chondrocytes and synovial cells leads to inflammation and damage to joint tissues, resulting in the severe arthralgia characteristic of the disease. Endothelial cell infection can disrupt the vascular barrier, contributing to edema and, in rare cases, hemorrhagic manifestations. Monocytes and macrophages serve as reservoirs for viral replication, facilitating viral dissemination to other tissues and organs. The tropism of MAYV is influenced by the expression of host cell receptors (such as Mxra8 and IRF3) and viral factors (such as E2 glycoprotein mutations), which can alter the virus's ability to infect different cell types and hosts (e.g., adapting to urban mosquito vectors or enhancing replication in human cells).
After an incubation period of 3-12 days, symptoms begin abruptly.
Acute Phase (Weeks 1-2): High fever (>39°C), severe headache, retro-orbital pain, myalgia, marked arthralgia (often affecting wrists, ankles, and fingers), and a maculopapular rash on the trunk and limbs. Gastrointestinal symptoms (nausea, vomiting, diarrhea) are common.
Convalescent Phase (Months to Years): The defining feature is the prolonged and debilitating polyarthralgia, which can persist for months or even years in a significant subset of patients (30-50%), resembling chikungunya disease. Fatigue and depression often accompany chronic joint pain.
| Epidemiology and Transmission Cycle | Details |
| Enzootic (Sylvatic) Cycle | MAYV is maintained in a primary forest cycle involving non-human primates (e.g., marmosets, capuchin monkeys) as reservoir/amplification hosts and canopy-dwelling mosquitoes of the genus Haemagogus as the principal vectors. |
| Spillover and Emergent Urban Cycle | Humans become infected when they encroach on these forest habitats (e.g., through deforestation, agriculture, recreation), acting as dead-end hosts. Alarmingly, urban spillover is now documented. Infected humans can introduce the virus into urban areas, where it may be transmitted by the highly efficient and widespread urban mosquitoes Aedes aegypti and Aedes albopictus. Laboratory studies confirm these vectors are competent for MAYV transmission, posing a risk for sustained urban epidemics akin to CHIKV and dengue. |
| Geographic Distribution and Risk | MAYV is endemic throughout the Amazon Basin (Brazil, Peru, Bolivia, Venezuela, Suriname, French Guiana) and extending into Central America, the Caribbean (Trinidad, Haiti), and northern South America. Seroprevalence studies suggest human infections are vastly underreported. Climate change, deforestation, and urbanization are key drivers of its expanding risk profile. |
Mayaro virus is a paradigm of an emerging arbovirus at a critical ecological crossroads. Its demonstrated ability to cause debilitating disease and its potential for urban expansion via Aedes mosquitoes make it a clear and present danger to public health in the Americas and beyond. While significant challenges in diagnosis and control remain, advances in understanding its molecular virology and pathogenesis are illuminating promising pathways for intervention. A proactive, research-driven approach is essential to prevent MAYV from becoming the next global arboviral epidemic.
Reference
| Target | Cat. No. | Product Name | Host | |
| MAYV | DAGA-270 | Mayaro virus E1 glycoprotein (aa 1-413) [His] | E. coli | Inquiry |
| MAYV | DAGA-271 | Mayaro virus E2 glycoprotein (aa 1-364) [His] | E. coli | Inquiry |
| MAYV | DAGC023 | Recombinant Mayaro Virus virus-like particles antigen | HEK293 cells | Inquiry |
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