Respiratory syncytial virus infection in human immunodeficiency virus-infected children

Chandwani, Sulachni; Borkowsky, William; Krasinski, Keith; Lawrence, Robert M.; Welliver, Robert C.

doi:10.1016/s0022-3476(05)80539-6

Cited by 108 publications

(45 citation statements)

References 12 publications

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“…Two of the 16 patients (12.5%) died of respiratory failure due to RSV pneumonia, despite intensive care unit admission and supportive ventilation (1). Immunosuppression caused by human immunodeficiency virus also affects RSV pathogenesis, and patients with AIDS have an increased duration of viral shedding (26).…”

Section: Disease In Immunosuppressed Individualsmentioning

confidence: 99%

Immune Responses and Disease Enhancement during Respiratory Syncytial Virus Infection

2005

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Respiratory syncytial virus (RSV) is one of the commonest and most troublesome viruses of infancy. It causes most cases of bronchiolitis, which is associated with wheezing in later childhood. In primary infection, the peak of disease typically coincides with the development of specific T- and B-cell responses, which seem, in large part, to be responsible for disease. Animal models clearly show that a range of immune responses can enhance disease severity, particularly after vaccination with formalin-inactivated RSV. Prior immune sensitization leads to exuberant chemokine production, an excessive cellular influx, and an overabundance of cytokines during RSV challenge. Under different circumstances, specific mediators and T-cell subsets and antibody-antigen immune complex deposition are incriminated as major factors in disease. Animal models of immune enhancement permit a deep understanding of the role of specific immune responses in RSV disease, assist in vaccine design, and indicate which immunomodulatory therapy might be beneficial to children with bronchiolitis

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Section: Disease In Immunosuppressed Individualsmentioning

confidence: 99%

Immune Responses and Disease Enhancement during Respiratory Syncytial Virus Infection

2005

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“…The cytotoxic cell response to RSV is important in controlling infection. Studies in patients having cellular immune deficiencies have shown that cellular immunity is important in protecting from severe RSV disease and limiting virus shedding (23,24). Studies in mice have shown that both CD4 ϩ and CD8 ϩ T cells are involved in terminating RSV replication, with CD8 ϩ T cells having a dominant role (25,26), and that the M2, F, and N proteins are the major targets for CTL (27)(28)(29).…”

Section: R Espiratory Syncytial Virus (Rsv)mentioning

confidence: 99%

Respiratory Syncytial Virus G Protein and G Protein CX3C Motif Adversely Affect CX3CR1+ T Cell Responses

Harcourt

Alvarez

Jones

et al. 2006

The Journal of Immunology

130

132

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Interactions between fractalkine (CX3CL1) and its receptor, CX3CR1, mediate leukocyte adhesion, activation, and trafficking. The respiratory syncytial virus (RSV) G protein has a CX3C chemokine motif that can bind CX3CR1 and modify CXCL1-mediated responses. In this study, we show that expression of the RSV G protein or the G protein CX3C motif during infection is associated with reduced CX3CR1+ T cell trafficking to the lung, reduced frequencies of RSV-specific, MHC class I-restricted IFN-γ-expressing cells, and lower numbers of IL-4- and CX3CL1-expressing cells. In addition, we show that CX3CR1+ cells constitute a major component of the cytotoxic response to RSV infection. These results suggest that G protein and the G protein CX3C motif reduce the antiviral T cell response to RSV infection.

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“…The protective role of antibodies in human disease is probably best demonstrated by the correlation between higher levels of maternally acquired antibodies and less serious disease in infants (9,10) and the ability of high titered RSV intravenous immunoglobulin (Ig) to decrease the risk of serious disease when administered prophylactically (15). The longer duration and severe complications of RSV infection in patients with reduced cellular immunity demonstrate the role of cellular immunity in clearing the infection (16,17).…”

Section: Introductionmentioning

confidence: 99%

Immune response to respiratory syncytial virus in young Brazilian children

Queiróz

Durigon

Botosso

et al. 2002

Braz J Med Biol Res

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We have evaluated the cellular and humoral immune response to primary respiratory syncytial virus (RSV) infection in young infants. Serum specimens from 65 patients £12 months of age (39 males and 26 females, 28 cases <3 months and 37 cases ³3 months; median 3 ± 3.9 months) were tested for anti-RSV IgG and IgG subclass antibodies by EIA. Flow cytometry was used to characterize cell surface markers expressed on peripheral blood mononuclear cells (PBMC) from 29 RSV-infected children. There was a low rate of seroconversion in children <3 months of age, whose acute-phase PBMC were mostly T lymphocytes (63.0 ± 9.0%). In contrast, a higher rate of seroconversion was observed in children >3 months of age, with predominance of B lymphocytes (71.0 ± 17.7%). Stimulation of PBMC with RSV (2 x 10 5 TCID 50 ) for 48 h did not induce a detectable increase in intracellular cytokines and only a few showed a detectable increase in RSVspecific secreted cytokines. These data suggest that age is an important factor affecting the infants' ability to develop an immune response to RSV.

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Respiratory syncytial virus infection in human immunodeficiency virus-infected children

Cited by 108 publications

References 12 publications

Immune Responses and Disease Enhancement during Respiratory Syncytial Virus Infection

Immune Responses and Disease Enhancement during Respiratory Syncytial Virus Infection

Respiratory Syncytial Virus G Protein and G Protein CX3C Motif Adversely Affect CX3CR1+ T Cell Responses

Immune response to respiratory syncytial virus in young Brazilian children

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