Preexisting antibodies can protect against congenital cytomegalovirus infection in monkeys.

Human cytomegalovirus (HCMV) is the most common congenital infection and a known cause of microcephaly, sensorineural hearing loss, and cognitive impairment among newborns worldwide. Natural maternal HCMV immunity reduces the incidence of congenital infection, but does not prevent the disease altogether. We employed a nonhuman primate model of congenital CMV infection to investigate the ability of preexisting antibodies to protect against placental CMV transmission in the setting of primary maternal infection and subsequent viremia, which is required for placental virus exposure.

Plasmablast Response to Primary Rhesus Cytomegalovirus (CMV) Infection in a Monkey Model of Congenital CMV Transmission.

Human cytomegalovirus (HCMV) is the most common congenital infection worldwide and the leading infectious cause of neurologic deficits and hearing loss in newborns. Development of a maternal HCMV vaccine to prevent vertical virus transmission is a high priority, yet protective maternal immune responses following acute infection are poorly understood. To characterize the maternal humoral immune response to primary CMV infection, we investigated the plasmablast and early antibody repertoire using a nonhuman primate model with two acutely rhesus CMV (RhCMV)-infected animals-a CD4 T cell-depleted dam that experienced fetal loss shortly after vertical RhCMV transmission and an immunocompetent dam that did not transmit RhCMV to her infant.

Maternal Antibody Responses and Nonprimary Congenital Cytomegalovirus Infection of HIV-1-Exposed Infants.

Risk of congenital cytomegalovirus (cCMV) transmission is highly dependent on the presence of preexisting maternal immunity, with the lowest rates observed in CMV-seroimmune populations. Among infants of CMV-seroimmune women, those who are exposed to human immunodeficiency virus (HIV) have an increased risk of acquiring cCMV infection as compared to HIV-unexposed infants. To better understand the risk factors of nonprimary cCMV transmission in HIV-infected women, we performed a case-control study in which CMV-specific plasma antibody responses from 19 CMV-transmitting and 57 CMV-nontransmitting women with chronic CMV/HIV coinfection were evaluated for the ability to predict the risk of cCMV infection.

Maternal CD4+ T cells protect against severe congenital cytomegalovirus disease in a novel nonhuman primate model of placental cytomegalovirus transmission.

Elucidation of maternal immune correlates of protection against congenital cytomegalovirus (CMV) is necessary to inform future vaccine design. Here, we present a novel rhesus macaque model of placental rhesus CMV (rhCMV) transmission and use it to dissect determinants of protection against congenital transmission following primary maternal rhCMV infection. In this model, asymptomatic intrauterine infection was observed following i.

Perinatal cytomegalovirus and varicella zoster virus infections: epidemiology, prevention, and treatment.

Mother-to-child transmission of cytomegalovirus (CMV) and varicella zoster virus (VZV) can lead to severe birth defects and neurologic impairment of infants. Congenital CMV complicates up to 1% of all pregnancies globally. Although antiviral treatment of infants congenitally infected with CMV can ameliorate the CMV-associated hearing loss and developmental delay, interventions to prevent congenital CMV infection and the associated neurologic impairments are still being evaluated.

Specific nucleoprotein residues affect influenza virus morphology.

Influenza virus strains are often pleiomorphic, a characteristic that is largely attributed to specific residues in matrix protein 1 (M1). Although the mechanism by which M1 controls virion morphology has not yet been defined, it is suggested that the M1 interaction with other viral proteins plays an important role. In this study, we rescued recombinant virus WSN-AichiM1 containing the spherical A/WSN/33 (WSN) backbone and the M1 protein from A/Aichi/2/68 (Aichi).

Specific residues in the 2009 H1N1 swine-origin influenza matrix protein influence virion morphology and efficiency of viral spread in vitro.

In April 2009, a novel influenza virus emerged as a result of genetic reassortment between two pre-existing swine strains. This highly contagious H1N1 recombinant (pH1N1) contains the same genomic background as North American triple reassortant (TR) viruses except for the NA and M segments which were acquired from the Eurasian swine lineage. Yet, despite their high degree of genetic similarity, we found the morphology of virions produced by the pH1N1 isolate, A/California/04/09 (ACal-04/09), to be predominantly spherical by immunufluorescence and electron microscopy analysis in human lung and swine kidney epithelial cells, whereas TR strains were observed to be mostly filamentous.