Large-scale testing of human serum to determine cytomegalovirus neutralising antibody

Leogrande, G; Merchionne, F.; Lazzarotto, Tiziana; Landini, Maria Paola

doi:10.1016/s0163-4453(05)80034-9

Cited by 9 publications

(3 citation statements)

References 20 publications

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“…The HCMV-NT 50 titers showed a weak to moderate correlation with EIA IgG-antibody titers in either virus–cell combination (Fig. 2 ), as reported previously [ 27 – 29 ]. When pregnant women are infected with HCMV as the primary infection, the IgG antibody, as determined by the EIA, become positive.…”

Section: Discussionsupporting

confidence: 87%

Association of human cytomegalovirus (HCMV) neutralizing antibodies with antibodies to the HCMV glycoprotein complexes

Shibamura

Yoshikawa

Yamada

et al. 2020

Virol J

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Background: Human cytomegalovirus (HCMV) causes asymptomatic infections, but also causes congenital infections when women were infected with HCMV during pregnancy, and life-threatening diseases in immunocompromised patients. To better understand the mechanism of the neutralization activity against HCMV, the association of HCMV NT antibody titers was assessed with the antibody titers against each glycoprotein complex (gc) of HCMV. Methods: Sera collected from 78 healthy adult volunteers were used. HCMV Merlin strain and HCMV clinical isolate strain 1612 were used in the NT assay with the plaque reduction assay, in which both the MRC-5 fibroblasts cells and the RPE-1 epithelial cells were used. Glycoprotein complex of gB, gH/gL complexes (gH/gL/gO and gH/gL/ UL128-131A [PC]) and gM/gN were selected as target glycoproteins. 293FT cells expressed with gB, gM/gN, gH/gL/ gO, or PC, were prepared and used for the measurement of the antibody titers against each gc in an indirect immunofluorescence assay (IIFA). The correlation between the IIFA titers to each gc and the HCMV-NT titers was evaluated. Results: There were no significant correlations between gB-specific IIFA titers and the HCMV-NT titers in epithelial cells or between gM/gN complex-specific IIFA titers and the HCMV-NT titers. On the other hand, there was a statistically significant positive correlation between the IIFA titers to gH/gL complexes and HCMV-NT titers. Conclusions: The data suggest that the gH/gL complexes might be the major target to induce NT activity against HCMV.

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Section: Discussionsupporting

confidence: 87%

Association of human cytomegalovirus (HCMV) neutralizing antibodies with antibodies to the HCMV glycoprotein complexes

Shibamura

Yoshikawa

Yamada

et al. 2020

Virol J

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“…For example, in human HCMV-convalescent sera there is only a poor correlation between virus-neutralizing capacity and ELISA titer. 41,42 In addition, the conventional ELISA systems specifically select for serum donors with high titers of antibodies against internal proteins that will never reach the surface of infected cells or represent virion components from the inner structures of the particle. Such antibodies can be expected to have little impact on direct virus neutralization or ADCC.…”

Section: Discussionmentioning

confidence: 99%

Protection from CMV infection in immunodeficient hosts by adoptive transfer of memory B cells

Klenovsek

Weisel²,

Schneider³

et al. 2007

Blood

106

102

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IntroductionCytomegalovirus (CMV) viremia and disease are a major cause of morbidity and mortality following hematopoietic stem cell transplantation (HSCT). 1,2 The most feared complication is CMV pneumonia, which is still associated with high mortality. 3 Preemptive therapy using antiviral drugs can reduce the incidence of early-onset CMV disease but is associated with substantial toxicity and development of late-onset CMV disease. 4,5 In addition, drugresistant virus strains might develop. 6 CMV replication in patients who underwent transplantation arises as a result of lack of immune control. Thus, bridging the period of immunodeficiency by passive transfer of the most important immune functions is a goal in transplantation medicine. Reports from the murine CMV model (MCMV) had established the importance of CD8 T cells for control of primary infection as well as latency. 7,8 Based on these findings, clinical protocols were developed whereby CD8 T-cell clones were cultured from the transplant donor and transferred to the patient after transplantation. [9][10][11] This strategy has proved effective in the prevention of reactivation and treatment of CMV infection that is unresponsive to antiviral therapy. 12 However, the MHC restriction of CD8 lymphocytes and the need to expand these cells in vitro makes this procedure cumbersome, and a limited number of patients has been treated so far. In addition, CD4 ϩ cells seem to be important for the long-term survival of the transferred CD8 cells. 9 More recently, CMV-specific CD8 ϩ T cells have been purified from the blood of stem cell transplant donors and infused directly into patients. 13 Measures have also been taken to support the humoral arm of the immune system. Again, data from the murine model of CMV have clearly demonstrated an important role of antibodies in protecting against a primary infection as well as reactivation or reinfection. 14,15 In contrast to T-cell transfer, support of the humoral immune system in patients has been limited to application of intravenous immune globulin (IVIG) or hyperimmune products. However, even after more than 20 years of extensive use of this treatment either prophylactically and/or therapeutically, uncertainty about benefits for the prevention of CMV infection and disease is evident. 16 Reasons are manifold but might include, among others, use of different products, 17 dosing regimens, and schedule. To our knowledge, cell-based strategies to support the humoral immune response in patients who underwent bone marrow transplantation (BMT) or HSCT have not been explored.In a mouse model, we have recently shown that virus-specific B cells that are adoptively transferred into immunodeficient hosts can be stimulated to antibody production by antigen alone; T-cell help is not required. 18 This finding suggested the possibility of prophylaxis and/or therapy of viral infections in T-celldeficient hosts by transfer of specific memory B cells. Here, we examine the protective capacity of adoptively transferred memory For personal use on...

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“…Unlike congenital rubella in which the damage incurred varies by gestational trimester, it presently is not known if time of infection is a factor in CMV damage. However, researchers (Leogrande, Merchionne, Lazzarotto, & Landini, 1992) suggested that there may be a direct relationship between the severity of neonatal infection and the time in gestational development at which CMV infection occurs. In addition, it has been suggested that congenital CMV may be an etiological agent in autism (Ivarsson, Bjerre, Vegfors, & Ahlfors, 1990).…”

mentioning

confidence: 99%

Cytomegalovirus.

Barona¹

1998

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OverviewCytomegalovirus (CMV) is a common herpes virus that infects between 50% and 85% of adults in the United States (Centers for Disease Control [CDCI, 1995). It is part of the same group that contains viruses that cause infectious mononucleosis (Epstein-Banvirus), chicken pox, and shingles (Children's Biomedical Research Institute [CBRII, 1989; CDC, 1995). For the most part, the virus remains nonsymptomatic with no long-term health implications (CBRI, 1989; CDC, 1995). However, CMV infection can have adverse outcomes for individuals with impaired immune systems or for the unborn children of the 1-3% of women who become infected for the first time during pregnancy (CDC, 1995;Marshall, Rabalais, Stewart, & Dobbins, 1993).CMV is the leading cause of infection in newborns (CDC, 1995). Approximately 1%, or 40,000 infants, are infected annually during gestation (Raynor, 1993), with up to 10% acquiring the virus during delivery or through breast milk (Adler, 1992;Minamishima et al., 1994). Complications of the virus are varied. Children who become infected with CMV after birth have few symptoms that, when they occur, resemble those of a generalized infection (CDC, 1995; Lajo, Borque, Del Castillo, & Martin-Ancel, 1994). In children infected in utero, complications may range from mild to severe. Although 85-90% of infants infected in utero are asymptomatic (CDC, 1995), these "clinically silent" children may be at risk for audiological, neurological, and developmental problems later in life (An dersen, 1988;Williamson, Demmler, Percy, & Catlin, 1992). The remaining 10-15% may experience neurological damage such as hearing impairments, psychomotor delays, and learning problems (CBRI, 1989;Raynor, 1993). In addition, some impairment in the visual, auditory, motor, and social areas may be progressive (CDC, 1995;O'Brien & Goldberg, 1992).The more severe forms of the disease affects approximately 1 in 1,000 US.-born infants (CBRI, 1989) and is fatal for approximately 30% (Jones & Isaacs, 1995;Raynor, 1993). Clinical manifestations include microcephaly (abnormal smallness of the head or cranial area), jaundice (yellow skin, tissue, and body fluid pigmentation caused by bile deposits), liver and spleen infection, pneumonia, cardiac anomaly, chorioretinitis, and CMV mononucleosis (CBRI, 1989). The most severe manifestation, cytomegalic 2 13

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Large-scale testing of human serum to determine cytomegalovirus neutralising antibody

Cited by 9 publications

References 20 publications

Association of human cytomegalovirus (HCMV) neutralizing antibodies with antibodies to the HCMV glycoprotein complexes

Association of human cytomegalovirus (HCMV) neutralizing antibodies with antibodies to the HCMV glycoprotein complexes

Protection from CMV infection in immunodeficient hosts by adoptive transfer of memory B cells

Cytomegalovirus.

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