ABSTRACT Background: Over-the-counter use of ivermectin amongst other drugs as SARS-CoV-2 treatment has been increasingly common, despite the lack of evidence on its clinical efficacy. Objective: To evaluate the effect of ivermectin use on production of antibodies against SARS-CoV-2 in health care workers (HCW) diagnosed with COVID-19 and of Th1/Th2 cytokines by stimulated peripheral blood mononuclear cells of the same cohort (PBMCs). Methods: This cross-sectional study evaluated seroconversion and neutralizing antibodies production in HCW at Complexo Hospitalar Universitário Professor Edgard Santos (Salvador, Brazil), diagnosed with COVID-19 from May to July, 2020, as well as in vitro production of antibody against SARS-CoV-2 and Th1/Th2 cytokines. Analyses were performed between December 2020 and February 2021. Participants were stratified according to the use of ivermectin (≤ 1 dose vs. multiple doses) for treatment of COVID-19. Results: 45 HCW were included (62% women). Mean age was 39 years, and disease severity was similar across groups. Neutralizing antibodies were detected less frequently in multiple doses (70%) vs. ≤ 1 dose (97%) groups, p = 0.02). PBMCs of patients in multiple doses group also were less likely to produce antibodies against SARS-CoV-2 following in vitro stimulation with purified spike protein in comparison with patients in ≤ 1 dose group (p < 0.001). PBMC’s production of Th1/Th2 cytokines levels was similar across groups. Abdominal pain (15% vs 46%, p = 0.04), diarrhea (21% vs. 55%, p = 0.05) and taste perversion (0% vs. 18%, p = 0.05) were more frequently reported by participants that used multiple doses of ivermectin. Conclusions: Although there was no evidence for differential disease severity upon ivermectin use for treatment of COVID-19 it was associated with more gastro-intestinal side-effects and impairment of anti-SARS-CoV2 antibodies production, in a dose dependent manner. This potentially impacts the effectiveness of immune response and the risk of reinfection and warrants additional studies for clarifying the mechanisms and consequences of such immunomodulatory effects.

Resumo Objetivo: descrever as expansões temporal e geográfica da circulação do vírus Zika (ZIKV) em países e territórios, desde seu isolamento até 2018. Métodos: revisão não sistemática da literatura do período entre 1947 e 2018, utilizando a base MEDLINE e estimativas da Organização Mundial da Saúde. Resultados: desde seu isolamento em 1947, a circulação do ZIKV expandiu-se pela África, Ásia e Pacífico, até chegar à América em 2013, causando manifestações clínicas graves; as maiores soroprevalências foram registradas na ilha de Yap (74%) e no Brasil (63%); mutações genéticas, a ausência de imunidade e a alta susceptibilidade dos vetores podem ter influenciado sua transmissibilidade e ajudam a explicar a magnitude de sua expansão. Conclusão: a expansão da circulação do ZIKV nas Américas foi a mais ampla já registrada, possivelmente resultado de características populacionais e geográficas dos locais por onde o vírus circulou.

Abstract Objective: to describe the temporal and geographical expansion of Zika virus (ZIKV) circulation in countries and territories, from the time it was first isolated until 2018. Methods: This was a non-systematic literature review covering the period from 1947 to 2018 using the MEDLINE database and World Health Organization estimates. Results: Since its isolation in 1947, ZIKV circulation spread through Africa, Asia and the Pacific before reaching the Americas in 2013, causing serious clinical manifestations; the highest seroprevalence rates were recorded in Yap (74%) and in Brazil (63%); genetic mutations, absence of immunity and high vector susceptibility may have influenced ZIKV transmissibility and help to explain the magnitude of its expansion. Conclusion: The spread of ZIKV circulation in the Americas was the most extensive recorded thus far, possibly as a result of population and geographical characteristics of the sites where the virus circulated.

Resumen Objetivo: Describir las expansiones temporal y geográfica de la circulación del virus Zika en países y territorios, desde su aislamiento hasta 2018. Métodos: Revisión no sistemática de la literatura del período comprendido entre 1947 y 2018 utilizando la base MEDLINE y estimaciones de la Organización Mundial de la Salud. Resultados: Desde su aislamiento en 1947 la circulación del virus Zika se expandió por África, Asia y el Pacífico hasta llegar a América en 2013, causando manifestaciones clínicas graves. Las mayores seroprevalencias se registraron en la isla Yap (74%) y en Brasil (63%). Mutaciones genéticas, ausencia de inmunidad y alta susceptibilidad de los vectores pueden haber influenciado su transmisibilidad y ayudan a explicar la magnitud de su expansión. Conclusión: La expansión de la circulación del virus Zika en las Américas fue la más amplia ya registrada, posiblemente como resultado de características poblacionales y geográficas de los lugares por donde el virus circuló.

Resumo Objetivo: descrever as expansões temporal e geográfica da circulação do vírus Zika (ZIKV) em países e territórios, desde seu isolamento até 2018. Métodos: revisão não sistemática da literatura do período entre 1947 e 2018, utilizando a base MEDLINE e estimativas da Organização Mundial da Saúde. Resultados: desde seu isolamento em 1947, a circulação do ZIKV expandiu-se pela África, Ásia e Pacífico, até chegar à América em 2013, causando manifestações clínicas graves; as maiores soroprevalências foram registradas na ilha de Yap (74%) e no Brasil (63%); mutações genéticas, a ausência de imunidade e a alta susceptibilidade dos vetores podem ter influenciado sua transmissibilidade e ajudam a explicar a magnitude de sua expansão. Conclusão: a expansão da circulação do ZIKV nas Américas foi a mais ampla já registrada, possivelmente resultado de características populacionais e geográficas dos locais por onde o vírus circulou.

Abstract Objective: to describe the temporal and geographical expansion of Zika virus (ZIKV) circulation in countries and territories, from the time it was first isolated until 2018. Methods: This was a non-systematic literature review covering the period from 1947 to 2018 using the MEDLINE database and World Health Organization estimates. Results: Since its isolation in 1947, ZIKV circulation spread through Africa, Asia and the Pacific before reaching the Americas in 2013, causing serious clinical manifestations; the highest seroprevalence rates were recorded in Yap (74%) and in Brazil (63%); genetic mutations, absence of immunity and high vector susceptibility may have influenced ZIKV transmissibility and help to explain the magnitude of its expansion. Conclusion: The spread of ZIKV circulation in the Americas was the most extensive recorded thus far, possibly as a result of population and geographical characteristics of the sites where the virus circulated.

Resumen Objetivo: Describir las expansiones temporal y geográfica de la circulación del virus Zika en países y territorios, desde su aislamiento hasta 2018. Métodos: Revisión no sistemática de la literatura del período comprendido entre 1947 y 2018 utilizando la base MEDLINE y estimaciones de la Organización Mundial de la Salud. Resultados: Desde su aislamiento en 1947 la circulación del virus Zika se expandió por África, Asia y el Pacífico hasta llegar a América en 2013, causando manifestaciones clínicas graves. Las mayores seroprevalencias se registraron en la isla Yap (74%) y en Brasil (63%). Mutaciones genéticas, ausencia de inmunidad y alta susceptibilidad de los vectores pueden haber influenciado su transmisibilidad y ayudan a explicar la magnitud de su expansión. Conclusión: La expansión de la circulación del virus Zika en las Américas fue la más amplia ya registrada, posiblemente como resultado de características poblacionales y geográficas de los lugares por donde el virus circuló.

Abstract A Zika virus seroepidemiology study was performed in 1084 blood donors collected from August to October 2015 in six sites of Cameroon representing a large panel of eco-environments. Samples were tested using an anti-NS1 IgG ELISA detection kit and positives were further confirmed by seroneutralization. The observed global seroprevalence was low (around 5%, peaking at 10% and 7.7% in Douala and Bertoua, respectively) with risk factors associated with seropositivity pointing to the existence of a local (peri-)sylvatic cycle of transmission. These results call attention to the potential introduction and subsequent spread in African urban areas of Asian genotype Zika virus currently circulating in the Americas and adapted to transmission by peri-domestic mosquitoes. They should leverage reinforced surveillance efforts in Africa.

Introduction:The human hepatitis B virus causes acute and chronic hepatitis and is considered one of the most serious human health issues by the World Health Organization, causing thousands of deaths per year. There are similar viruses belonging to the Hepadnaviridae family that infect non-human primates and other mammals as well as some birds. The majority of non-human primate virus isolates were phylogenetically close to the human hepatitis B virus, but like the human genotypes, the origins of these viruses remain controversial. However, there is a possibility that human hepatitis B virus originated in primates. Knowing whether these viruses might be common to humans and primates is crucial in order to reduce the risk to humans.Objective:To review the existing knowledge about the evolutionary origins of viruses of the Hepadnaviridae family in primates.Methods:This review was done by reading several articles that provide information about the Hepadnaviridae virus family in non-human primates and humans and the possible origins and evolution of these viruses.Results:The evolutionary origin of viruses of the Hepadnaviridae family in primates has been dated back to several thousand years; however, recent analyses of genomic fossils of avihepadnaviruses integrated into the genomes of several avian species have suggested a much older origin of this genus.Conclusion:Some hypotheses about the evolutionary origins of human hepatitis B virus have been debated since the '90s. One theory suggested a New World origin because of the phylogenetic co-segregation between some New World human hepatitis B virus genotypes F and H and woolly B virus in basal sister-relationship to the Old monkey human hepatitis World non-human primates and human hepatitis B virus variants. Another theory suggests an Old World origin of human hepatitis B virus, and that it would have been spread following prehistoric human migrations over 100,000 years ago. A third theory suggests a co-speciation of human hepatitis B virus in non-human primate hosts because of the proximity between the phylogeny of Old and New World non-human primate and their human hepatitis B virus variants. The importance of further research, related to the subject in South American wild fauna, is paramount and highly relevant for understanding the origin of human hepatitis B virus.

IntroductionDespite hepatocytes being the target cells of hepatitis C virus (HCV), viral ribonucleic acid RNA has been detected in other cells, including platelets, which have been described as carriers of the virus in the circulation of infected patients. Platelets do not express cluster differentiation 81 CD81, the main receptor for the virus in hepatocytes, although this receptor protein has been found in megakaryocytes. Still, it is not clear if HCV interacts with platelets directly or if this interaction is a consequence of its association with megakaryocytes. The aim of this study was to evaluate the interaction of HCV with platelets from non-infected individuals, after in vitro exposure to the virus.MethodsPlatelets obtained from 50 blood donors not infected by HCV were incubated in vitro at 37°C for 48h with serum containing 100,000IU∕mL of genotype 1 HCV. After incubation, RNA extracted from the platelets was assayed for the presence of HCV by reverse transcription – polymerase chain reaction RT-PCR.ResultsAfter incubation in the presence of virus, all samples of platelets showed HCV RNA.ConclusionsThe results demonstrate that, in vitro, the virus interacts with platelets despite the absence of the receptor CD81, suggesting that other molecules could be involved in this association.