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Introdução/objetivos: Infecções pelo ZIKV ocasionalmente podem desencadear um amplo espectro de malformações congênitas, coletivamente denominados de Síndrome da Zika Congênita. Um número restrito de estudos descreve a imunidade na infecção pelo ZIKV durante a gravidez, tanto em modelos experimentais, como em pacientes. Desta forma, buscamos determinar se a resposta imunológica de memória específica ao ZIKV, 2 a 3 anos após a infecção primária, desenvolvida por mães infectadas durante a gravidez e de seus filhos expostos ao vírus por via transplacentária é efetiva e duradoura. Métodos: A resposta efetora de linfócitos T de vinte e uma mães e dezoito crianças foi avaliada por ELISPOT de IFN- γ e citometria de fluxo após estimulação com megapools de ZIKV. Resultados: Como principais achados, observamos uma alta frequência de linfócitos T CD4+ de perfil Th2 efetora/memória e de linfócitos T CD8+ de perfil Th1 naive, seguida de linfócitos T CD8+ de perfil Tc2 efetora/memória nas mães e crianças, indicando que essas células estariam, de alguma forma, auxiliando a resposta imune humoral de mães e crianças com histórico de infecção pelo ZIKV. Observamos ainda, que a capacidade de degranulação e produção de IFN-γ pelos linfócitos T CD4+ foram detectadas nos três grupos de pacientes mesmo após 2-3 anos de infecção, indicando que os linfócitos T CD4+ mantém um perfil de memória de longa duração. Por outro lado, as habilidades de degranulação e produção de IFN-γ pelos linfócitos T CD8+ foram ausentes ou baixos nos três grupos de pacientes após o mesmo período, indicando que os linfócitos T CD8+ mantém um perfil de memória de curta duração quando comparado aos T CD4+. Por fim, demonstramos que os linfócitos T CD4+ TEMRA são os principais produtores de IFN-γ. Conclusão: É importante relembrar que embora não estejamos estudando a infecção aguda na gestação, nossos dados refletem um imprint do que provavelmente ocorreu na infecção aguda. Desta forma, nosso estudo descreve pontos importantes de relevância imunológica, clínica e epidemiológica, particularmente em relação aos linfócitos T CD8+ de memória específicos ao ZIKV que são gerados, mas mantidos por um curto período. Também evidenciarmos que as respostas de linfócitos T específicas ao ZIKV nas mães parecem não ter sido diferenciadas na fase aguda e que, portanto, não estariam relacionadas ao desfecho clínico dos bebês.

This study was conducted to provide information on the genetic diversity of human parvovirus B19 (B19V) circulating in the municipality of Niterói, Rio de Janeiro, Southeast Brazil during 1996–2006, a period with two distinct outbreaks of B19V infection: 1999–2000 and 2004–2005. A total of 27 sera from patients with erythema infectiosum and five sera from HIV-infected patients that tested positive for B19V DNA during the study period were analyzed. To genotype B19V strains, a semi-nested PCR for partial amplification of the capsid gene was performed and sequence analysis revealed that 31 sequences belonged to subgenotype 1a (G1a) of the main genotype 1 and one sequence was characterized as subgenotype 3b (G3b). The phylogenetic tree supported the division of the G1a into two well-defined clades with 1.3% of divergence. The low diversity of the G1a strains may be explained by the fact that all patients had acute B19V infection and 30/32 sera were collected during two distinct outbreaks. The G3b strain was from an HIV-infected patient who seroconverted to anti-B19 IgG antibodies in September/2005. This is the first report of G3b in the state of Rio de Janeiro. Keywords: B19V genotypes, Outbreak, Erythema infectiosum, Brazil

Objective: Compare the anti-T. gondii IgG titer between HIV-1 infected and non HIV-1 infected pregnant women and report three cases of congenital toxoplasmosis resulting from reactivation of infection during pregnancy of HIV-1 infected women. Methods: This study was conducted among 2,270 pregnant women with chronic Toxoplasma gondii infection (absence of IgM and presence of IgG), including 82 HIV-1 infected and 2,188 non-infected women. Results: The average anti-T. gondii IgG titer was 127 for the 2,188 non-HIV-1 infected women, and 227 for the 82 HIV-1-infected women (p = 0,007). These results suggested that higher anti-T. gondii IgG titers in HIV-1-infected pregnant women may not be indicative of an elevated risk for fetal infection. In this study three cases of congenital toxoplasmosis that resulted from infection reactivation during pregnancy of HIV-1-infected women were manifested by fetal death, symptomatic infection, and infant without symptoms, respectively. In two of these women, a ten-fold increase in IgG levels above used cutoff was observed (2,320 UI/mL and 3,613 UI/mL, respectively). In the third pregnant women anti-T. gondii IgG titers during pregnancy did not rise despite the occurrence of congenital toxoplasmosis (204; 198; 172 UI/mL). Conclusions: Congenital toxoplasmosis resulting reactivation of infection during pregnancy in the studied group leads us to believe that it is a public health problem, especially in our population, in which seroprevalence of T. gondii infections is high. These findings also suggest that special attention is necessary during pregnancy, because the serologic diagnosis may not be indicative of toxoplasmosis reactivation. Keywords: Toxoplasma, Toxoplasmosis, congenital, HIV infections

We report the occurrence of congenital toxoplasmosis in three infants born to HIV infected women who had high anti-toxoplasma IgG and negative IgM during pregnancy. We briefly reviewed available literature and discussed the possible transmission mechanisms of congenital toxoplasmosis among HIV infected pregnant women. Serum samples were tested for Toxoplasma gondii IgM and IgG antibodies using commercial enzyme immunoassay and IgG-avidity tests. In the first case, fetal death occurred at 28th week of gestation. In the second case, congenital toxoplasmosis was diagnosis at 6th month of life; and in the third case, an HIV-infected newborn, congenital toxoplasmosis was asymptomatic. These cases point out to the possibility of enhanced maternal-fetal transmission of T. gondii infection by HIV-infected women chronically infected, which may have important public health consequences, considering that increasing frequency of HIV-infection has been observed among women of childbearing age around the world. Keywords: congenital toxoplasmosis, human immunodeficiency-virus, prevention, AIDS

We report the occurrence of congenital toxoplasmosis in three infants born to HIV infected women who had high anti-toxoplasma IgG and negative IgM during pregnancy. We briefly reviewed available literature and discussed the possible transmission mechanisms of congenital toxoplasmosis among HIV infected pregnant women. Serum samples were tested for Toxoplasma gondii IgM and IgG antibodies using commercial enzyme immunoassay and IgG-avidity tests. In the first case, fetal death occurred at 28th week of gestation. In the second case, congenital toxoplasmosis was diagnosis at 6th month of life; and in the third case, an HIV-infected newborn, congenital toxoplasmosis was asymptomatic. These cases point out to the possibility of enhanced maternal-fetal transmission of T. gondii infection by HIV-infected women chronically infected, which may have important public health consequences, considering that increasing frequency of HIV-infection has been observed among women of childbearing age around the world.

OBJECTIVE: Compare the anti-T. gondii IgG titer between HIV-1 infected and non HIV-1 infected pregnant women and report three cases of congenital toxoplasmosis resulting from reactivation of infection during pregnancy of HIV-1 infected women. METHODS: This study was conducted among 2,270 pregnant women with chronic Toxoplasma gondii infection (absence of IgM and presence of IgG), including 82 HIV-1 infected and 2,188 non-infected women. RESULTS: The average anti-T. gondii IgG titer was 127 for the 2,188 non-HIV-1 infected women, and 227 for the 82 HIV-1-infected women (p = 0,007). These results suggested that higher anti-T. gondii IgG titers in HIV-1-infected pregnant women may not be indicative of an elevated risk for fetal infection. In this study three cases of congenital toxoplasmosis that resulted from infection reactivation during pregnancy of HIV-1-infected women were manifested by fetal death, symptomatic infection, and infant without symptoms, respectively. In two of these women, a ten-fold increase in IgG levels above used cutoff was observed (2,320 UI/mL and 3,613 UI/mL, respectively). In the third pregnant women anti-T. gondii IgG titers during pregnancy did not rise despite the occurrence of congenital toxoplasmosis (204; 198; 172 UI/mL). CONCLUSIONS: Congenital toxoplasmosis resulting reactivation of infection during pregnancy in the studied group leads us to believe that it is a public health problem, especially in our population, in which seroprevalence of T. gondii infections is high. These findings also suggest that special attention is necessary during pregnancy, because the serologic diagnosis may not be indicative of toxoplasmosis reactivation.

Human parvovirus B19 infection can cause erythema infectiosum (EI) and several other clinical presentations. Central nervous system (CNS) involvement is rare, and only a few reports of encephalitis and aseptic meningitis have been published. Here, we describe 2 cases of B19 infection in a family presenting different clinical features. A 30 year old female with a 7-day history of headache, malaise, myalgias, joint pains, and rash was seen. Physical examination revealed a maculopapular rash on the patient's body, and arthritis of the hands. She completely recovered in 1 week. Two days before, her 6 year old son had been admitted to a clinic with a 1-day history of fever, headache, abdominal pain and vomiting. On admission, he was alert, and physical examination revealed neck stiffness, Kerning and Brudzinski signs, and a petechial rash on his trunk and extremities. Cerebrospinal fluid analysis was normal. He completely recovered in 5 days. Acute and convalescent sera of both patients were positive for specific IgM antibody to B19. Human parvovirus B19 should be considered in the differential diagnosis of aseptic meningitis, particularly during outbreaks of erythema infectiosum. The disease may mimic meningococcemia and bacterial meningitis.