o'nyong-nyong virus envelope protein 2; ONNV E2 protein; ONNV E2; o'nyong'nyong virus protein E2; ONNV Envelope Antigen 2; ONNV
Purity
>95% , based on SDS PAGE
Format
Liquid
Concentration
Batch dependent - please inquire should you have specific requirements.
Buffer
In PBS with 8M Urea
Preservative
None
Storage
Stable for 6 months at -20˚C from the date of shipment. Nonhazardous. No MSDS required.
Antigen Description
The o'nyong'nyong virus or o'nyong-nyong virus (ONNV) is a virus first isolated by the Uganda Virus Research Institute in Entebbe, Uganda in 1959. It is a togavirus (family Togaviridae), genus Alphavirus and is closely related to the chikungunya and Igbo
Keywords
o'nyong-nyong virus envelope protein 2;ONNV E2 protein;ONNV E2;o'nyong'nyong virus protein E2;ONNV Envelope Antigen 2;ONNV
Citations
Publication ()
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Background
O'nyong nyong virus (ONNV) was first isolated in Uganda in 1959 and spread to southeastern Africa in 1963, where it is now mainly endemic south of the Sahara. The virus is arboviral and can cause severe joint pain when it infects humans, hence the local name for the disease, o'nyong-nyong. ONNV belongs to the family Togaviridae, genus Alphavirus. The genus Alphavirus contains an important group of arboviruses with a wide geographic distribution and therefore different evolutionary trajectories, which are categorized as "old world" and "new world" viruses based on genome sequence comparisons and geographic location. ONNV is closely related to other members of the Old World virus family, such as Chikungunya virus (CHIKV), Mayaro virus (MAYV), and Ross River virus (RRV), all of which are known for their characteristic arthralgia symptoms.
ONNV has overlapping epidemiological areas with CHIKV, but the two have different vectors. CHIKV is primarily transmitted by aedine mosquitoes, while the primary vector for ONNV is Anopheles mosquitoes. ONNV is transmitted alternately between arthropod and vertebrate hosts, causing long-term persistent infection in mosquitoes, and blood-borne transmission through mosquito bites can cause short-term acute infections in vertebrates.
Figure 1. Epidemiology of ONNV (Source: Tong Jia Ming S, et al. 2024)
Human infection with ONNV initially presents with fever, large arthralgias, headache, generalized maculopapular rash, posterior cervical lymphadenopathy, and conjunctivitis. It is difficult to make a differential diagnosis with chikungunya fever based on clinical manifestations alone. Laboratory diagnosis also requires caution because of the high serologic cross-reactivity between the two. The virus can be isolated from the patient's blood during the first week of illness, and viral RNA can be detected by reverse transcription polymerase chain reaction. ONNV serum IgM antibody levels are detectable from the second week of illness and persist for 2 months. The reciprocal plaque reduction neutralization test (PRNT) distinguishes ONNV from CHIKV in humoral immunity.
1. Tong Jia Ming S, et al. Pathogenicity and virulence of O'nyong-nyong virus: A less studied Togaviridae with pandemic potential. Virulence. 2024 Dec;15(1):2355201.
2. Rezza G, et al. O'nyong-nyong fever: a neglected mosquito-borne viral disease. Pathog Glob Health. 2017 Sep;111(6):271-275.
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Arboviruses are public health threats that cause explosive outbreaks. Major determinants of arbovirus transmission, geographic spread, and pathogenesis are the magnitude and duration of viremia in vertebrate hosts. Previously, we determined that multiple alphaviruses are cleared efficiently from murine circulation by the scavenger receptor MARCO (Macrophage receptor with collagenous structure). Here, we define biochemical features on chikungunya (CHIKV), o'nyong 'nyong (ONNV), and Ross River (RRV) viruses required for MARCO-dependent clearance in vivo. In vitro, MARCO expression promotes binding and internalization of CHIKV, ONNV, and RRV via the scavenger receptor cysteine-rich (SRCR) domain. Furthermore, we observe species-specific effects of the MARCO SRCR domain on CHIKV internalization, where those from known amplification hosts fail to promote CHIKV internalization. Consistent with this observation, CHIKV is inefficiently cleared from the circulation of rhesus macaques in contrast with mice. These findings suggest a role for MARCO in determining whether a vertebrate serves as an amplification or dead-end host following CHIKV infection.
FHL1 promotes chikungunya and o'nyong-nyong virus infection and pathogenesis with implications for alphavirus vaccine design
Nat Commun
Authors: Ng WH, Liu X, Ling ZL, Santos CNO, Magalhães LS, Kueh AJ, Herold MJ, Taylor A, Freitas JR, Koit S, Wang S, Lloyd AR, Teixeira MM, Merits A, Almeida RP, King NJC, Mahalingam S.
Arthritogenic alphaviruses are positive-strand RNA viruses that cause debilitating musculoskeletal diseases affecting millions worldwide. A recent discovery identified the four-and-a-half-LIM domain protein 1 splice variant A (FHL1A) as a crucial host factor interacting with the hypervariable domain (HVD) of chikungunya virus (CHIKV) nonstructural protein 3 (nsP3). Here, we show that acute and chronic chikungunya disease in humans correlates with elevated levels of FHL1. We generated FHL1-/- mice, which when infected with CHIKV or o'nyong-nyong virus (ONNV) displayed reduced arthritis and myositis, fewer immune infiltrates, and reduced proinflammatory cytokine/chemokine outputs, compared to infected wild-type (WT) mice. Interestingly, disease signs were comparable in FHL1-/- and WT mice infected with arthritogenic alphaviruses Ross River virus (RRV) or Mayaro virus (MAYV). This aligns with pull-down assay data, which showed the ability of CHIKV and ONNV nsP3 to interact with FHL1, while RRV and MAYV nsP3s did not. We engineered a CHIKV mutant unable to bind FHL1 (CHIKV-ΔFHL1), which was avirulent in vivo. Following inoculation with CHIKV-ΔFHL1, mice were protected from disease upon challenge with CHIKV and ONNV, and viraemia was significantly reduced in RRV- and MAYV-challenged mice. Targeting FHL1-binding as an approach to vaccine design could lead to breakthroughs in mitigating alphaviral disease.
COA
Publication 
Figure 1. Epidemiology of ONNV
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