History of the Cytomegalovirus

Riley, Harris D.

doi:10.1097/00007611-199702000-00004

Cited by 27 publications

(15 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Cytomegalovirus (CMV) and Parvovirus B19 (PB19) are viruses implicated commonly in the pathogenesis of fetal loss [Horn and Rose, 1998;Van den Veyver et al, 1998;Embleton, 2001;Syridou et al, 2005]. PB19 has been reported as the cause of spontaneous abortion, intrauterine fetal death, and non-immune hydrops fetalis [Heegaard and Brown, 2002], whereas CMV has been reported to cause non-immune hydrops fetalis, intrauterine growth retardation and congenital defects [Riley, 1997;Antsaklis et al, 2000]. In addition, apart from neonatal or congenital disease, herpes simplex virus types 1 and 2 (HSV-1/2) infection during pregnancy may lead to preterm delivery, intrauterine growth retardation, non-immune hydrops fetalis or fetal loss, even though the incidence is rare [Brown et al, 1987;Vasileiadis et al, 2003].…”

Section: Introductionmentioning

confidence: 99%

“…Most of the reports concerning adverse pregnancy outcomes following viral infection during gestation have several limitations, because the cases selected for study usually have specific characteristics such as occurrence of non-immune hydrops fetalis or maternal infection caused by a specific virus, which has been proven by serology antenatally [Brown et al, 1987;Riley, 1997;Antsaklis et al, 2000;Heegaard and Brown, 2002;Vasileiadis et al, 2003]. In the present study, cases of fetal loss were examined for CMV, PB19, and HSV-1/2 infection by molecular assays of placental tissues and compared with a control term delivery population.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Detection of cytomegalovirus, parvovirus B19 and herpes simplex viruses in cases of intrauterine fetal death: Association with pathological findings

Syridou

Spanakis

Konstantinidou

et al. 2008

Journal of Medical Virology

View full text Add to dashboard Cite

There are previous indications that transplacental transmission of cytomegalovirus (CMV), parvovirus B19 (PB19) and herpes simplex virus types 1 and 2 (HSV-1/2) cause fetal infections, which may lead to fetal death. In a prospective case-control study we examined the incidence of these viruses in intrauterine fetal death and their association with fetal and placenta pathological findings. Molecular assays were performed on placenta tissue extracts of 62 fetal deaths and 35 controls for the detection of CMV, PB19 and HSV-1/2 genomes. Formalin-fixed, paraffin-embedded liver, spleen and placenta tissues of fetal death cases were evaluated histologically. Thirty-four percent of placental specimens taken from intrauterine fetal deaths were positive for any of the three viruses (16%, 13%, and 5% positive for CMV, PB19, and HSV-1/2, respectively), whereas only 6% of those taken from full term newborns were positive (P = 0.0017). No dual infection was observed. This difference was also observed when fetal deaths with a gestational age <20 weeks or a gestational age >20 weeks were compared with the controls (P = 0.025 and P = 0.0012, respectively). Intrauterine death and the control groups differed in the detection rate of CMV DNA (16% and 3%, respectively; P = 0.047), which was more pronounced in a gestational age >20 weeks (P = 0.03). Examination of the pathological findings among the PCR-positive and PCR-negative fetal deaths revealed that hydrops fetalis and chronic villitis were more common among the former group (P = 0.0003 and P = 0.0005, respectively). In conclusion, an association was detected between viral infection and fetal death, which was more pronounced in the advanced gestational age. Fetal hydrops and chronic villitis were evidently associated with viral DNA detection in cases of intrauterine death.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Detection of cytomegalovirus, parvovirus B19 and herpes simplex viruses in cases of intrauterine fetal death: Association with pathological findings

Syridou

Spanakis

Konstantinidou

et al. 2008

Journal of Medical Virology

View full text Add to dashboard Cite

show abstract

“…Cells infected with CMV were first described pathologically in the late 1800s, with accounts of “cytomegalic cells with intranuclear inclusions” (Riley,1997; Ho,2008). Several cases of “cytomegalic inclusion disease” were described in infants in the early 20th century (Hanshaw,1966; Ho,2008), but it wasn't until the advent of cell culture technology that the causative agent, subsequently named cytomegalovirus , was first isolated in 1956 and 1957 (Rowe et al,1956; Smith,1956; Craig et al,1957).…”

Section: Introductionmentioning

confidence: 99%

“…Several cases of “cytomegalic inclusion disease” were described in infants in the early 20th century (Hanshaw,1966; Ho,2008), but it wasn't until the advent of cell culture technology that the causative agent, subsequently named cytomegalovirus , was first isolated in 1956 and 1957 (Rowe et al,1956; Smith,1956; Craig et al,1957). The availability of diagnostic testing for CMV increased knowledge of its epidemiology and resulted in expansion of the phenotype of congenitally infected infants, including a better understanding of the effects of CMV on infants who are asymptomatic at birth (Riley,1997).…”

Section: Introductionmentioning

confidence: 99%

Teratology: From science to birth defects prevention

Rasmussen

Erickson

Reef

et al. 2008

Birth Defects Research

View full text Add to dashboard Cite

One of the goals of birth defects research is to better understand risk or preventive factors for birth defects so that strategies for prevention can be developed. In this article, we have selected four areas of birth defects research that have led to the development of prevention strategies. These areas include rubella virus as a cause of congenital rubella syndrome, folic acid as a preventive factor for neural tube defects, cytomegalovirus infection as a cause of birth defects and developmental disabilities, and alcohol as a cause of fetal alcohol spectrum disorders. For each of these areas, we review key clinical and research findings that led to the identification of the risk or preventive factor, milestones in the development of prevention strategies, and the progress made thus far toward prevention.

show abstract

“…Among the non-primate CMVs, the most thoroughly studied virus is the MCMV (Davison & Bhella, 2007, Redwood et al, 2008). (Griffiths, 2006;Riley, 1997) (Mocarski et al, 2015). In 1960, Weller proposed that the virus, previously only described as "salivary gland viruses", be called after its cytopathologic effect (Mocarski et al, 2015;Griffiths, 2006).…”

Section: Cytomegalovirus (Cmv)mentioning

confidence: 99%

Cell-type specific activities of cytomegalovirus GPCR homologues

Oliveira¹

View full text Add to dashboard Cite

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 ...

show abstract

History of the Cytomegalovirus

Cited by 27 publications

References 0 publications

Detection of cytomegalovirus, parvovirus B19 and herpes simplex viruses in cases of intrauterine fetal death: Association with pathological findings

Detection of cytomegalovirus, parvovirus B19 and herpes simplex viruses in cases of intrauterine fetal death: Association with pathological findings

Teratology: From science to birth defects prevention

Cell-type specific activities of cytomegalovirus GPCR homologues

Contact Info

Product

Resources

About