Seroconversion to Human Herpesvirus 6 and Human Herpesvirus 7 Among Brazilian Children with Clinical Diagnoses of Measles or Rubella

Black, Jodi B.; Durigon, Edison Luiz; Kite-Powell, Kathleen; Souza, Luiza de Marilac de; Curli, Sueli P.; Afonso, Anna Maria Sardinha; Theobaldo, Márcia; Pellett, Philip E.

doi:10.1093/clinids/23.5.1156

Cited by 33 publications

(12 citation statements)

References 11 publications

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“…Exanthem subitum is often misdiagnosed as measles or rubella (Black et al, 1996a;Tait et al, 1996;Oliveira et al, 2003) despite its typical clinical features (Juretic, 1963) and the rash has also been confused with allergic reactions to antibiotics (Irving et al, 1990). As regards less easily recognised febrile illnesses, the seminal work of Hall et al (1994) showed that primary HHV-6 infection accounted for 20% of fevers between 6 and 12 months of age.…”

Section: Background-the Need For Diagnosismentioning

confidence: 99%

The natural history and laboratory diagnosis of human herpesviruses-6 and -7 infections in the immunocompetent

Ward

2005

Journal of Clinical Virology

152

151

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Section: Background-the Need For Diagnosismentioning

confidence: 99%

The natural history and laboratory diagnosis of human herpesviruses-6 and -7 infections in the immunocompetent

Ward

2005

Journal of Clinical Virology

152

151

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“…More commonly a mixture of pathogenic bacteria is identified [37] but when a single etiology can be identified the most common pathogens identified include Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus [37] [38] [39] [40]. It has also been suggested that MV infection is associated with reactivation of latent Mycobacterium tuberculosis infections [41] and has been linked to reactivation of latent herpes virus infections [42].…”

Section: Clinical Observations In Acute Measles Virus Patientsmentioning

confidence: 99%

Mechanisms of Measles Virus-Induced Immune Suppression in the Cotton Rat Model

Carsillo

2010

Journal of Interferon & Cytokine Research

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The World Health Organization estimates that ~200,000 people, the majority of them children, died in 2007 following acute measles. Bacterial pneumonia following virus-induced immune suppression is one of the leading fatal complications of acute measles virus (MV) infection. Despite its clinical importance, the underlying mechanisms of MV-induced immunosuppression remain unresolved. To study MV-induced immune suppression we use the cotton rat, because it is the only rodent shown to replicate MV in the respiratory tract after intranasal infection and to develop T-cell proliferation inhibition, a hallmark of MV-induced immune suppression. Enhanced pulmonary susceptibility to secondary bacterial infection in MV-infected patients is well established. This might indicate a defect in the macrophage response, as these cells play an important role in immune responses against bacterial infections through phagocytosis and microbicidal activity as well as through cytokine production and the stimulation and modulation of T-helper cell responses.To test the effect of MV on macrophages in vitro , we have established a method to culture cotton rat macrophages. Cotton rat bone marrow-derived macrophages are phenotypically and functionally more similar to human than rodent macrophages because they secrete little nitric oxide. After infection with measles virus, macrophages produce less IL-12 than uninfected macrophages. Based on studies in humans, it has been hypothesized that the lack of IL-12 might lead to a T-helper type 2 (TH2) response, which might be mechanistically linked to immune suppression. In cotton rats, IL-12 secretion was suppressed after infection with both wild-type and vaccine virus. After stimulation of spleen or lymph node cells with MV antigen, only IFN-g was detected, indicative of a TH1 response. Cytokines compatible with a mixed TH0 response, IFN and IL-4, were detectable in supernatants after stimulation with PMA/ionomycin. A recombinant vaccine virus that secretes cotton rat IL-4 was used to investigate the contribution of a TH2 response to immune suppression. This virus enhanced IL-4 secretion but did not increase T-cell proliferation inhibition. These data show that measles virus infection leads to a decrease in IL-12 secretion and an increase in IL-4 secretion but this does not seem to correlate with development of a TH2 response and immune suppression.Inhibition of T-cell proliferation following MV infection results from down-regulation of AKT kinase activity. AKT is also a key signaling molecule in a number of pathways for primary macrophage functions. In cotton rats, wild-type and vaccine MV infection leads to a down-regulation of AKT activity in macrophages concurrent with decreased phagocytosis and bacterial killing, and increased susceptibility to Staphylococcus aureus pneumonia in vivo .Contrary to MV, many viruses activate the PI3K-AKT signaling pathway as a strategy to slow down apoptosis and increase virus replication. Our data indicate that an increased level of active AKT kinase does not si...

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“…Further aggravated by malnutrition, secondary infections then often follow a severe or fatal course (Dollimore et al, 1997). Furthermore, persistent infections by other pathogens may be reactivated or exacerbated as a result of MV-induced immunosuppression in children and young adults (Black et al, 1996;Tamashiro et al, 1987). MV was the first pathogen noted to cause immunosuppression, almost a century ago, when von Pirquet first coined the term 'anergy' to describe immunological impairment in a clinical condition when he described the transient loss of delayed-type hypersensitivity responses to tuberculin during measles.…”

Section: Measles Virus: the T-cell Silencing Conceptmentioning

confidence: 99%

Silencing T cells or T-cell silencing: concepts in virus-induced immunosuppression

Schneider‐Schaulies

Dittmer

2006

Journal of General Virology

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The ability to evade or suppress the host's immune response is a property of many viruses, indicating that this provides an advantage for the pathogen to spread efficiently or even to establish a persistent infection. The type and complexity of its genome and cell tropism but also its preferred type of host interaction are important parameters which define the strategy of a given virus to modulate the immune system in an optimal manner. Because they take a central position in any antiviral defence, the activation and function of T cells are the predominant target of many viral immunosuppressive regimens. In this review, two different strategies whereby this could be achieved are summarized. Retroviruses can infect professional antigen-presenting cells and impair their maturation and functional properties. This coincides with differentiation and expansion of silencing T cells referred to as regulatory T cells with suppressive activity, mainly to CD8 + effector T cells. The second concept, outlined for measles virus, is a direct, contact-mediated silencing of T cells which acquire a transient paralytic state. Retroviruses: the silencing T-cell concept One hallmark of many retroviral infections is a severe virus-induced immunosuppression. For example, human

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Seroconversion to Human Herpesvirus 6 and Human Herpesvirus 7 Among Brazilian Children with Clinical Diagnoses of Measles or Rubella

Cited by 33 publications

References 11 publications

The natural history and laboratory diagnosis of human herpesviruses-6 and -7 infections in the immunocompetent

The natural history and laboratory diagnosis of human herpesviruses-6 and -7 infections in the immunocompetent

Mechanisms of Measles Virus-Induced Immune Suppression in the Cotton Rat Model

Silencing T cells or T-cell silencing: concepts in virus-induced immunosuppression

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