Stability of SARS-CoV-2 and other airborne viruses under different stress conditions.

Viral stability under stress conditions may directly affect viral dissemination, seasonality, and pathogenesis. We exposed airborne viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), mumps virus, coxsackievirus B5, human rhinovirus A16, and respiratory syncytial virus, to different temperatures, UV light exposure time, pH values, and osmotic pressures and measured the remaining viral infectivity. Reduced thermal stability was observed for coxsackievirus B5 at 45 °C, while SARS-CoV-2 demonstrated residual infectivity at 55 °C. UV light exposure was an efficient means of viral inactivation but was less efficient for non-enveloped viruses. Rhinovirus A16 and respiratory syncytial virus demonstrated extreme sensitivity to acid conditions, while SARS-CoV-2, rhinovirus A16, and respiratory syncytial virus were unstable in an alkaline environment. The information obtained in this study will be useful for the development of viral inactivation methods and may be correlated with epidemiological and seasonal viral characteristics.

Chikungunya Virus Exposure Partially Cross-Protects against Mayaro Virus Infection in Mice.

Chikungunya virus (CHIKV) and Mayaro virus (MAYV) are closely related members of the Semliki Forest virus antigenic complex classified as belonging to the genus Alphavirus of the family Togaviridae. These viruses cause human disease, with sudden fever and joint inflammation that can persist for long periods. CHIKV is the causative agent of large outbreaks worldwide, and MAYV infection represents a growing public health concern in Latin America, causing sporadic cases and geographically limited outbreaks. Considering the relationship between CHIKV and MAYV, the present study aimed to evaluate if preexisting CHIKV immunity protects against MAYV infection. Immunocompetent C57BL/6 mice were intraperitoneally infected with CHIKV and, 4 weeks later, they were infected with MAYV in their hind paw. We observed that the preexistence of CHIKV immunity conferred partial cross-protection against secondary MAYV infection, reducing disease severity, tissue viral load, and histopathological scores. Interestingly, CHIKV antibodies from humans and mice showed low cross-neutralization to MAYV, but neutralizing activity significantly increased after secondary infection. Furthermore, depletion of adaptive immune cells (CD4+ T, CD8+ T, and CD19+ B cells) did not alter the cross-protection phenotype, suggesting that distinct cell subsets or a combination of adaptive immune cells stimulated by CHIKV are responsible for the partial cross-protection against MAYV. The reduction of proinflammatory cytokines, such as interferon gamma (IFN-γ), in animals secondarily infected by MAYV, suggests a role for innate immunity in cross-protection. Our findings shed light on how preexisting immunity to arthritogenic alphaviruses may affect secondary infection, which may further develop relevant influence in disease outcome and viral transmission. IMPORTANCE Mosquito-borne viruses have a worldwide impact, especially in tropical climates. Chikungunya virus has been present mostly in developing countries, causing millions of infections, while Mayaro virus, a close relative, has been limited to the Caribbean and tropical regions of Latin America. The potential emergence and spread of Mayaro virus to other high-risk areas have increased the scientific community's attention to an imminent worldwide epidemic. Here, we designed an experimental protocol of chikungunya and Mayaro virus mouse infection, which develops a measurable and quantifiable disease that allows us to make inferences about potential immunological effects during secondary virus infection. Our results demonstrate that previous chikungunya virus infection is able to reduce the severity of clinical outcomes during secondary Mayaro infection. We provide scientific understanding of immunological features during secondary infection with the closely related virus, thus assisting in better comprehending viral transmission and the pathological outcome of these diseases.

Lying in wait: the resurgence of dengue virus after the Zika epidemic in Brazil.

After the Zika virus (ZIKV) epidemic in the Americas in 2016, both Zika and dengue incidence declined to record lows in many countries in 2017-2018, but in 2019 dengue resurged in Brazil, causing ~2.1 million cases. In this study we use epidemiological, climatological and genomic data to investigate dengue dynamics in recent years in Brazil. First, we estimate dengue virus force of infection (FOI) and model mosquito-borne transmission suitability since the early 2000s. Our estimates reveal that DENV transmission was low in 2017-2018, despite conditions being suitable for viral spread. Our study also shows a marked decline in dengue susceptibility between 2002 and 2019, which could explain the synchronous decline of dengue in the country, partially as a result of protective immunity from prior ZIKV and/or DENV infections. Furthermore, we performed phylogeographic analyses using 69 newly sequenced genomes of dengue virus serotype 1 and 2 from Brazil, and found that the outbreaks in 2018-2019 were caused by local DENV lineages that persisted for 5-10 years, circulating cryptically before and after the Zika epidemic. We hypothesize that DENV lineages may circulate at low transmission levels for many years, until local conditions are suitable for higher transmission, when they cause major outbreaks.

Systems analysis of subjects acutely infected with the Chikungunya virus.

The largest ever recorded epidemic of the Chikungunya virus (CHIKV) broke out in 2004 and affected four continents. Acute symptomatic infections are typically associated with the onset of fever and often debilitating polyarthralgia/polyarthritis. In this study, a systems biology approach was adopted to analyze the blood transcriptomes of adults acutely infected with the CHIKV. Gene signatures that were associated with viral RNA levels and the onset of symptoms were identified. Among these genes, the putative role of the Eukaryotic Initiation Factor (eIF) family genes and apolipoprotein B mRNA editing catalytic polypeptide-like (APOBEC3A) in the CHIKV replication process were displayed. We further compared these signatures with signatures induced by the Dengue virus infection and rheumatoid arthritis. Finally, we demonstrated that the CHIKV in vitro infection of murine bone marrow-derived macrophages induced IL-1 beta production in a mechanism that is significantly dependent on the inflammasome NLRP3 activation. The observations provided valuable insights into virus-host interactions during the acute phase and can be instrumental in the investigation of new and effective therapeutic interventions.

Infection with Saint Louis encephalitis virus in the city of Ribeirao Preto, Brazil: report of one case.

Saint Louis encephalitis virus (SLEV) is a mosquito-borne flavivirus from the Americas. In this report we describe aspects of the laboratory diagnosis of a patient with an acute febrile illness induced by SLEV that was initially diagnosed as dengue by positive IgM-ELISA. Infection with this virus is probably not rare in Brazil, but cases remain undiagnosed. It is necessary to improve the surveillance system, including laboratories, for the diagnosis of SLEV in Brazil.

DENV-3 genotype III circulating in São Paulo, Brazil,from 2003 to 2008 is not associated with dengue haemorrhagic fever/dengue shock syndrome.

Dengue viruses (DENV) are the most important arboviruses of public health significance, and compriseof four distinct antigenic serotypes (DENV-1 to 4) that show substantial genetic diversity. These virusesusually cause dengue fever (DF) but some patients progress to a more severe form of the illness, i.e.dengue haemorrhagic fever/dengue shock syndrome (DHF/DSS). The first reports of DENV-3 cases inBrazil occurred in the year 2000 with co-circulation of DENV-1 and 2. Thereafter, DENV-3 spreadthroughout the country. DENV-3 phylogenetic analysis has revealed the existence of four to five DENV-3 genotypes. Genotype III of DENV-3 has been the main genotype circulating in Brazil, but recent studieshave indicated that DENV-3 genotype I and genotype V are also circulating in some states of Brazil. Inorder to evaluate DENV-3 genotypes circulating in São Paulo state from 2003 through 2008 we analyzedthe NS1 region of DENV-3 isolated from patients residing in Ribeirão Preto and presenting with differentclinical manifestations of dengue disease. Nucleotide sequences from 31 viruses were obtained andcompared to 105 DENV-3 corresponding sequences retrieved from GenBank. Phylogenetic analysisshowed that São Paulo DENV-3 sequences belong to genotype III and that Puerto Rico strains are closelyrelated to South American strains. There was no association between DENV-3 genotype and DHF/DSS.