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Testing the intrinsic mechanisms driving the dynamics of Ross River Virus across Australia.

ABSTRACT: The mechanisms driving dynamics of many epidemiologically important mosquito-borne pathogens are complex, involving combinations of vector and host factors (e.g., species composition and life-history traits), and factors associated with transmission and reporting. Understanding which intrinsic mechanisms contribute most to observed disease dynamics is important, yet often poorly understood. Ross River virus (RRV) is Australia's most important mosquito-borne disease, with variable transmission dynamics across geographic regions. We used deterministic ordinary differential equation models to test mechanisms driving RRV dynamics across major epidemic centers in Brisbane, Darwin, Mandurah, Mildura, Gippsland, Renmark, Murray Bridge, and Coorong. We considered models with up to two vector species (Aedes vigilax, Culex annulirostris, Aedes camptorhynchus, Culex globocoxitus), two reservoir hosts (macropods, possums), seasonal transmission effects, and transmission parameters. We fit models against long-term RRV surveillance data (1991-2017) and used Akaike Information Criterion to select important mechanisms. The combination of two vector species, two reservoir hosts, and seasonal transmission effects explained RRV dynamics best across sites. Estimated vector-human transmission rate (average β = 8.04x10-4per vector per day) was similar despite different dynamics. Models estimate 43% underreporting of RRV infections. Findings enhance understanding of RRV transmission mechanisms, provide disease parameter estimates which can be used to guide future research into public health improvements and offer a basis to evaluate mitigation practices.

SUBMITTER: Koolhof IS

PROVIDER: S-EPMC10868856 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature

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Testing the intrinsic mechanisms driving the dynamics of Ross River Virus across Australia.

Koolhof Iain S IS Beeton Nicholas N Bettiol Silvana S Charleston Michael M Firestone Simon M SM Gibney Katherine K Neville Peter P Jardine Andrew A Markey Peter P Kurucz Nina N Warchot Allan A Krause Vicki V Onn Michael M Rowe Stacey S Franklin Lucinda L Fricker Stephen S Williams Craig C Carver Scott S

PLoS pathogens 20240215 2

The mechanisms driving dynamics of many epidemiologically important mosquito-borne pathogens are complex, involving combinations of vector and host factors (e.g., species composition and life-history traits), and factors associated with transmission and reporting. Understanding which intrinsic mechanisms contribute most to observed disease dynamics is important, yet often poorly understood. Ross River virus (RRV) is Australia's most important mosquito-borne disease, with variable transmission dy ...[more]

PMID: 38358961

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Project description:BackgroundThe automated monitoring of routinely collected disease surveillance data has the potential to ensure that important changes in disease incidence are promptly recognised. However, few studies have established whether the signals produced by automated monitoring methods correspond with events considered by epidemiologists to be of public health importance. This study investigates the correspondence between retrospective epidemiological evaluation of notifications of Ross River virus (RRv) disease in Western Australia, and the signals produced by two cumulative sum (cusum)-based automated monitoring methods.MethodsRRv disease case notification data between 1991 and 2004 were assessed retrospectively by two experienced epidemiologists, and the timing of identified outbreaks was compared with signals generated from two different types of cusum-based automated monitoring algorithms; the three Early Aberration Reporting System (EARS) cusum algorithms (C1, C2 and C3), and a negative binomial cusum.ResultsWe found the negative binomial cusum to have a significantly greater area under the receiver operator characteristic curve when compared with the EARS algorithms, suggesting that the negative binomial cusum has a greater level of agreement with epidemiological opinion than the EARS algorithms with respect to the existence of outbreaks of RRv disease, particularly at low false alarm rates. However, the performance of individual EARS and negative binomial cusum algorithms were not significantly different when timeliness was also incorporated into the area under the curve analyses.ConclusionOur retrospective analysis of historical data suggests that, compared with the EARS algorithms, the negative binomial cusum provides greater sensitivity for the detection of outbreaks of RRv disease at low false alarm levels, and decreased timeliness early in the outbreak period. Prospective studies are required to investigate the potential usefulness of these algorithms in practice.

Project description:Ross River virus (RRV) is one of a group of mosquito-transmitted alphaviruses that cause debilitating, and often chronic, musculoskeletal disease in humans. Previously, we reported that replacement of the nonstructural protein 1 (nsP1) gene of the mouse-virulent RRV strain T48 with that from the mouse-avirulent strain DC5692 generated a virus that was attenuated in a mouse model of disease. Here we find that the six nsP1 nonsynonymous nucleotide differences between strains T48 and DC5692 are determinants of RRV virulence, and we identify two nonsynonymous nucleotide changes as sufficient for the attenuated phenotype. RRV T48 carrying the six nonsynonymous DC5692 nucleotide differences (RRV-T48-nsP1(6M)) was attenuated in both wild-type and Rag1(-/-) mice. Despite the attenuated phenotype, RRV T48 and RRV-T48-nsP1(6M) loads in tissues of wild-type and Rag1(-/-) mice were indistinguishable from 1 to 3 days postinoculation. RRV-T48-nsP1(6M) loads in skeletal muscle tissue, but not in other tissues, decreased dramatically by 5 days postinoculation in both wild-type and Rag1(-/-) mice, suggesting that the RRV-T48-nsP1(6M) mutant is more sensitive to innate antiviral effectors than RRV T48 in a tissue-specific manner. In vitro, we found that the attenuating mutations in nsP1 conferred enhanced sensitivity to type I interferon. In agreement with these findings, RRV T48 and RRV-T48-nsP1(6M) loads were similar in mice deficient in the type I interferon receptor. Our findings suggest that the type I IFN response controls RRV infection in a tissue-specific manner and that specific amino acid changes in nsP1 are determinants of RRV virulence by regulating the sensitivity of RRV to interferon.Arthritogenic alphaviruses, including Ross River virus (RRV), infect humans and cause debilitating pain and inflammation of the musculoskeletal system. In this study, we identified coding changes in the RRV nsP1 gene that control the virulence of RRV and its sensitivity to the antiviral type I interferon response, a major component of antiviral defense in mammals. Furthermore, our studies revealed that the effects of these attenuating mutations are tissue specific. These findings suggest that these mutations in nsP1 influence the sensitivity of RRV to type I interferon only in specific host tissues. The new knowledge gained from these studies contributes to our understanding of host responses that control alphavirus infection and viral determinants that counteract these responses.

Project description:BackgroundRoss River virus (RRV), Australia's most notifiable vector-borne disease transmitted through mosquito bites, has seen increased transmission due to rising temperatures. Quantifying the burden of RRV infection attributable to increasing temperatures (both current and future) is pivotal to inform prevention strategies in the context of climate change.MethodsAs RRV-related deaths are rare in Australia, we utilised years lived with disability (YLDs) associated with RRV infection data from the Australian Institute of Health and Welfare (AIHW) Burden of Disease database between 2003 and 2018. We obtained relative risks per 1 °C temperature increase in RRV infection from a previous meta-analysis. Exposure distributions for each Köppen-Geiger climate zone were calculated separately and compared with the theoretical-minimum-risk exposure distribution to calculate RRV burden attributable to increasing temperatures during the baseline period (2003-2018), and projected future burdens for the 2030s and 2050s under two greenhouse gas emission scenarios (Representative Concentration Pathways, RCP 4.5 and RCP 8.5), two adaptation scenarios, and different population growth series.FindingsDuring the baseline period (2003-2018), increasing mean temperatures contributed to 35.8 (±0.5) YLDs (19.1%) of the observed RRV burden in Australia. The mean temperature attributable RRV burden varied across climate zones and jurisdictions. Under both RCP scenarios, the projected RRV burden is estimated to increase in the future despite adaptation scenarios. By the 2050s, without adaptation, the RRV burden could reach 45.8 YLDs under RCP4.5 and 51.1 YLDs under RCP8.5. Implementing a 10% adaptation strategy could reduce RRV burden to 41.8 and 46.4 YLDs, respectively.InterpretationThese findings provide scientific evidence for informing policy decisions and guiding resource allocation for mitigating the future RRV burden. The current findings underscore the need to develop location-specific adaptation strategies for climate-sensitive disease control and prevention.FundingAustralian Research Council Discovery Program.

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Testing the intrinsic mechanisms driving the dynamics of Ross River Virus across Australia.

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Testing the intrinsic mechanisms driving the dynamics of Ross River Virus across Australia.

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