Impaired Cellular Immunity to Cytomegalovirus in Congenitally Infected Children and Their Mothers

Starr, Stuart E.; Tolpin, Mark D.; Friedman, Harvey M.; Paucker, Kurt; Plotkin, Stanley А.

doi:10.1093/infdis/140.4.500

Cited by 102 publications

(39 citation statements)

References 13 publications

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“…This latter observation confirms previous studies' findings of long-lasting suppression of lymphocyte blastogenic responses to HCMV in adults after mononucleosis [25] and in adolescents after asymptomatic primary HCMV infection [4]. Similar findings were observed in babies with perinatal or postnatal HCMV infection [26,27], in congenitally infected children, and in their mothers [28][29][30][31].…”

Section: Discussionsupporting

confidence: 91%

Lymphoproliferative Response in Primary Human Cytomegalovirus (HCMV) Infection Is Delayed in HCMV Transmitter Mothers

et al. 2006

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Background. The T cell-mediated immune response to human cytomegalovirus (HCMV) after primary infection, as well as the determinants of intrauterine transmission, are poorly understood.Methods. Sequential peripheral blood leukocyte samples from 74 pregnant women and 29 nonpregnant individuals with primary infection were examined for HCMV-specific CD4 + T cells by cytokine flow cytometry (CFC) and lymphoproliferative response (LPR) analysis. Immunological results for 19 transmitter and 21 nontransmitter mothers were compared.Results. Comparison of CFC and LPR analysis results showed that (1) there was no difference between pregnant and nonpregnant individuals; (2) HCMV-specific CD4 + T cells were detected by CFC, in the absence of an LPR to HCMV, in the great majority or the totality (according to different intervals) of samples collected from both pregnant and nonpregnant individuals during follow-up; and (3) LPR to HCMV was significantly ( ) lowered or delayed in transmitter mothers, compared with that in nontransmitter mothers.Conclusions. Pregnancy does not influence the HCMV-specific immune response. A dissociation between CFC response and LPR is commonly observed in patients with primary infections, and ad hoc studies aimed at understanding the mechanism(s) of the reduced LPR in transmitter mothers are warranted.

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Section: Discussionsupporting

confidence: 91%

Lymphoproliferative Response in Primary Human Cytomegalovirus (HCMV) Infection Is Delayed in HCMV Transmitter Mothers

et al. 2006

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“…In cell culture, CMV is less destructive than other viruses known to infect man and this is probably related to its capacity to energize the host cell (Isom, 1979). The long term nature of CMV infections in young children, often amounting to the first years of life (Stagno et al, 1975), may be related to the longevity of infected cells in rico with possible protection from the host's immune response (Gehrz et al, 1977;Starr et al, 1979). Assuming cell viability, it is conceivable that infected cells could be rescued from virus control as a consequence of the action of selective antiviral drugs.…”

Section: Discussionmentioning

confidence: 99%

Fine Structure of Cells Infected with Human Cytomegalovirus After Treatment with 9-(1,3-Dihydroxy-2-propoxymethyl)guanine

Mobberley¹,

Ryder²,

Hart³

et al. 1987

Journal of General Virology

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SUMMARYInfection with human cytomegalovirus (CMV) is characterized by cytological changes which are readily visualized by electron microscopy using ultrathin sections of infected cells. Treatment of such cells with 9-(1,3-dihydroxy-2-propoxymethyl)guanine (DHPG), a potent inhibitor of CMV, is effective when initiated at early or late times after infection and the response to such treatment has been studied by fine structural analysis. Inhibition of viral DNA synthesis by DHPG treatment (50 laM) late in virus infi:ction resulted in a cessation of virus growth accompanied by a lack of development and possible regression in skein-like intranuclear inclusions together with a depletion in cytoplasmic dense bodies. Such changes were accompanied by the appearance of nuclear dense bodies. These were also present when virus growth was reduced (5 gM-DHPG) rather than completely inhibited (50 gM-DHPG) by treatment initiated from the time of infection. The nuclear bodies were predominantly of a reticular type structure after the early treatment but mainly of a homogeneous form when virus growth was interrupted at late times. Their presence appeared to be connected with the ability of infected cells to initiate the synthesis of late proteins and their morphology may relate to the extent of such protein synthesis. Unlike cytoplasmic dense bodies, provisional findings on the characterization of the nuclear bodies suggested that the 691( matrix protein was not present in abundance.

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“…Several studies have demonstrated previously that lymphocytes from patients with congenital CMV infection generally lack proliferative responses to CMV in vitro [Gehrz et al, 1977[Gehrz et al, , 1982Reynolds et al, 1979;Starr et al, 1979] and production of interferon (IFN) in response to CMV antigens [Gehrz and Leonard, 1985]. Impairment in antigen recognition appears to be CMV-specific because a proliferative response is exhibited to mitogens [Gehrz et al, 1977].…”

Section: Introductionmentioning

confidence: 99%

Flow cytometric analysis of cytomegalovirus‐specific cell‐mediated immunity in the congenital infection

Hayashi

Kimura

Morishima

et al. 2003

Journal of Medical Virology

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Flow cytometric analysis of CD4(+) and CD8(+) T cells specific to human cytomegalovirus (CMV) was undertaken in seven patients with congenital CMV infection, six healthy infants who had acquired infection, and six CMV-seropositive adults. Intracellular cytokine assays showed that 0.03-2.23% of CD4(+) T cells in the healthy infants and adults produced interferon-gamma (IFN-gamma) in response to CMV antigens. In contrast, such CD4(+) T cells were almost undetectable in patients with congenital CMV infection who were younger than 2 years of age. Tetrameric major histocompatibility complex/peptide complex analysis demonstrated HLA*A2402-restricted phosphoprotein 65-specific CD8(+) T cells to be present in most healthy infants and adults tested, but almost absent in the patients. Interestingly, CMV-specific CD4(+) T-cell responses were observed in two patients with congenital infection beyond the age of 5 years. The present study points to impairment of CMV-specific cellular immunity in patients in single-cell levels with congenital CMV infection during the infant period and possible restoration in later childhood.

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Impaired Cellular Immunity to Cytomegalovirus in Congenitally Infected Children and Their Mothers

Cited by 102 publications

References 13 publications

Lymphoproliferative Response in Primary Human Cytomegalovirus (HCMV) Infection Is Delayed in HCMV Transmitter Mothers

Lymphoproliferative Response in Primary Human Cytomegalovirus (HCMV) Infection Is Delayed in HCMV Transmitter Mothers

Fine Structure of Cells Infected with Human Cytomegalovirus After Treatment with 9-(1,3-Dihydroxy-2-propoxymethyl)guanine

Flow cytometric analysis of cytomegalovirus‐specific cell‐mediated immunity in the congenital infection

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