Congenital cytomegalovirus infection

Syggelou, Angeliki; Iacovidou, Nicoletta; Kloudas, S.; Christoni, Zoi; Papaevangelou, Vana

doi:10.1111/j.1749-6632.2010.05649.x

Cited by 43 publications

(35 citation statements)

References 20 publications

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“…Unlike most herpesviruses, primary HCMV infection in healthy individuals is frequently silent (Syggelou et al, 2010). Less frequently, it induces minor symptoms similar to those of influenza or mononucleosis, such as fever, lymphocytosis, pharyngitis, lymphadenopathy, hepatosplenomegaly, minor increase in transaminase levels.…”

Section: Human CMV Infectionmentioning

confidence: 99%

“…This is an important feature, since many antiviral drugs target the product of this gene. On the other hand, many genes that manipulate the host immune system have arisen over the time within the HCMV genome, like ULL111A, an interleukin-10 coding gene, or US28, a chemokine receptor coding gene Syggelou et al, 2010). Interestingly, many genes of different viral isolates may have a low level of similarity.…”

Section: Cytomegalovirus (Cmv)mentioning

confidence: 99%

“…The latter can undergo through two different situations: reactivation of a latent infection or infection with another HCMV strain (Boppana et al, 2001;Hyde et al, 2010;McDonagh et al, 2004;Wang et al, 2011). Maternal infected leukocytes allow viral access to permissive placental cells and amniotic fluid, which provide access to the foetus (Griffiths & Walter, 2005;Syggelou et al, 2010). Congenital infection can lead to severe permanent disabilities and to death.…”

Section: Congenital Infectionmentioning

confidence: 99%

“…Cells infected by the HCMV have distinct morphologic alterations: the virus induces an abnormal growth in the cell and generates marked and typical intracellular inclusions in both cytoplasm and nucleus, leading to the emergence of multinucleated giant cells (cytomegalia) (Syggelou et al, 2010) (ICTV, 2011). The morphology of the HCMV viral particle follows the architecture of a typical herpesvirus virion, adjusting, however, to the HCMV particularities.…”

Section: Cytomegalovirus (Cmv)mentioning

confidence: 99%

“…However, manifestations and sequelae are more severe in congenital infections caused by maternal primary infection than recurrent episode of infection Rahav et al, 2007;Syggelou et al, 2010). Nevertheless, the viral vertical transmission rate diverges greatly between the two groups, as the presence of antibodies can also represent a reducer factor of intrauterine transmission chances: while only in 0.2 to 1.8% of foetuses become infected with HCMV in seropositive mothers, the transmission rate of virus from mothers with primary infection during pregnancy is about 30 to 40% (Boppana et al, 2001;Kenneson & Cannon, 2007;Manicklal et al, 2013;Syggelou et al, 2010;Zalel et al, 2008) (CDC, 2016. There is one study, however, suggesting that although differences in vertical transmission rate exist and are high, they are not as high as it has been indicated, and both groups share similar rates of congenital infection (Rahav et al, 2007).…”

Section: Congenital Infectionmentioning

confidence: 99%

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Cell-type specific activities of cytomegalovirus GPCR homologues

Oliveira¹

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The human cytomegalovirus (HCMV) is the main agent of congenital infection worldwide. Although primary infections or reactivations do not represent a threat to most individuals, they impose a lifethreating event to a developing foetus or immunocompromised individuals. Although we have learnt much about sites of viral replication and cells involved in the end-stage disease, the specific pathway and essential cell types that the virus must go through to later establish a successful infection and latency is still not clear. HCMV encodes four GPCR homologues (vGPCR): US27, US28, UL33 and UL78. vGPCR have been implicated in viral pathogenesis due to their ability to activate signalling pathways and, thus, alter physiological processes to favour infection. US28 and UL33 have been shown to activate several kinases and transcriptional factors. A key component of both US28 and UL33 sequence is the DRY (Asp/Arg/Tyr) motif, a region directly involved with G protein binding.Because Gα protein content is cell type-dependent, signalling activation by vGPCR can differ from cell to cell. Furthermore, these receptors share the particular characteristic of being constitutively Functional studies demonstrated migration induction of HTR-8 following transfection by either US28 or UL33. In order to investigate potential mechanisms, signalling pathways were probed via detection of activated kinases and the secretion of matrix metalloproteinases (MMP) and chemokines (CK) via luminex assays. Although differences in the level of kinases could not be measured by western blot, induction of MMP and CK were detected by Luminex assays, with contrasting results for US28 and UL33 in transfected cells (HTR-8 and HUVEC). An HCMV recombinant disrupted for US28 signalling (DQY) was generated and compared with wild type HCMV and a US28 null mutant for induction of MMP and CK in virus-infected cells. US28-dependent effects were identified for infected human foreskin fibroblasts, but results for HUVEC were equivocal.iii To determine potential bottlenecks to viral dissemination that may require M33 function(s), mice were infected with M33 knockout (M33) viruses by different routes: intranasal, -mimicking the most natural route, footpad -a more compartmentalized route, and intraperitoneal, the most direct route to major organs. To help track viral dissemination, a luciferase tagged M33 was generated and infection was compared to control virus (M78luc). M33 intranasal infection did not result in attenuation for colonisation of the nose, draining (superficial cervical) lymph nodes (dLN) or the lungs. Via footpad route, M33 colonised the footpad and dLN to levels equivalent to control virus, but was significantly attenuated in spread to the spleen and, subsequently, the salivary glands.Following intraperitoneal infection, the virus is readily delivered to major organs due to direct access to the bloodstream, there was no difference in the colonisation of primary organs (spleen, liver) between M33 and control MCMV, but M33 was still unable ...

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Section: Human CMV Infectionmentioning

confidence: 99%

Section: Cytomegalovirus (Cmv)mentioning

confidence: 99%

Section: Congenital Infectionmentioning

confidence: 99%

Section: Cytomegalovirus (Cmv)mentioning

confidence: 99%

Section: Congenital Infectionmentioning

confidence: 99%

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Cell-type specific activities of cytomegalovirus GPCR homologues

Oliveira¹

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Prevalence of congenital cytomegalovirus infection in Slovenia: A study on 2,841 newborns

Paradiž

Seme

Puklavec

et al. 2011

Journal of Medical Virology

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Human cytomegalovirus (CMV) is the most frequent cause of congenital infection in humans. In the first prevalence study of congenital CMV infection in Eastern and Central Europe, all neonates born in a 22-month period in two Slovenian maternity units (total of 2,841 newborns) were screened prospectively for congenital CMV infection by a real-time polymerase chain reaction (PCR) in urine. In all newborns with positive screening results, plasma and dried blood spots (DBS) collected at birth were tested additionally for CMV DNA. Congenital CMV infection was confirmed by virus isolation from a urine sample collected within the first 2 weeks of life. Congenital CMV infection was identified in four out of 2,841 newborns tested (incidence 0.14%; 95% CI, 0.05-0.39%). In four newborns with confirmed congenital infection, the concentration of CMV DNA in urine ranged from 4.68 to 8.18 log(10) copies/ml, all four newborns had detectable CMV DNA in plasma taken at birth (1.26-3.34 log(10) copies/ml) and two out of four had detectable CMV DNA in DBS collected during newborn metabolic screening. None of the four newborns with confirmed congenital CMV infection was symptomatic. The study showed that the prevalence of congenital CMV infection at birth in Slovenia is among the lowest in the world and that CMV DNA PCR testing of urine is a suitable and affordable real-time screening strategy for congenital CMV infection. If it is performed in 24 mini-pools, the cost of screening is 1.4 €/newborn and the cost of detecting a single newborn with congenital CMV infection 1,000 €.

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