1994
DOI: 10.1002/jmv.1890430113
|View full text |Cite
|
Sign up to set email alerts
|

Tumor necrosis factor, interleukin‐2, and interferon‐gamma in adult varicella

Abstract: Adult varicella can be a severe illness complicated by pneumonia, encephalitis, or prolonged fever. This study measured levels of tumor necrosis factor (TNF)-alpha, interleukin-2 (IL-2), and interferon gamma (IFN-G) in a consecutive group of 31 adult varicella patients presenting within 24 hours of rash onset. All cytokines were assayed using an ELISA technique. TNF-alpha was detectable in 71% of patients with a mean level of 52 pg/ml. IL-2 was detectable in 29% with a mean level of 1040 pg/ml. IFN-gamma was d… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
9
0
1

Year Published

2000
2000
2023
2023

Publication Types

Select...
5
4

Relationship

1
8

Authors

Journals

citations
Cited by 26 publications
(10 citation statements)
references
References 10 publications
0
9
0
1
Order By: Relevance
“…VZV-specific T-cell recognition is critical for host recovery from varicella, and both MHC class I-restricted CD8 ϩ and MHC class IIrestricted CD4 ϩ T cells are sensitized during primary VZV infection. VZV-specific CD4 ϩ T cells that are elicited during primary infection are predominantly of the Th1 type (7, 54) and function to produce high levels of IFN-␥, which potentiates the clonal expansion of VZV-specific T cells (3,26,51). Although the classical cytotoxic T-lymphocyte (CTL) response is mediated by CD8 ϩ T cells that recognize viral peptides in association with MHC class I molecules, VZV-specific CTLs can also exhibit MHC class II (CD4 ϩ )-restricted killing of infected target cells (15,17,19,20,23,25,49).…”
Section: We Sought To Investigate the Effects Of Varicella-zoster Virmentioning
confidence: 99%
See 1 more Smart Citation
“…VZV-specific T-cell recognition is critical for host recovery from varicella, and both MHC class I-restricted CD8 ϩ and MHC class IIrestricted CD4 ϩ T cells are sensitized during primary VZV infection. VZV-specific CD4 ϩ T cells that are elicited during primary infection are predominantly of the Th1 type (7, 54) and function to produce high levels of IFN-␥, which potentiates the clonal expansion of VZV-specific T cells (3,26,51). Although the classical cytotoxic T-lymphocyte (CTL) response is mediated by CD8 ϩ T cells that recognize viral peptides in association with MHC class I molecules, VZV-specific CTLs can also exhibit MHC class II (CD4 ϩ )-restricted killing of infected target cells (15,17,19,20,23,25,49).…”
Section: We Sought To Investigate the Effects Of Varicella-zoster Virmentioning
confidence: 99%
“…Multiple components of the innate and antigen-specific immune responses are activated during the course of primary VZV infection. The early host responses to VZV are nonspecific and involve natural killer cells and interferons which function to restrict virus replication and spread (2,3,51). VZV-specific T-cell recognition is critical for host recovery from varicella, and both MHC class I-restricted CD8 ϩ and MHC class IIrestricted CD4 ϩ T cells are sensitized during primary VZV infection.…”
mentioning
confidence: 99%
“…It has also been noted that patients with acute varicella infection have high serum levels of TNF-a. 16 In vitro replication of VZV and its antigen expression are inhibited by TNF-a and this antiviral activity can be blocked by monoclonal antibodies against TNFa. 17 Therefore, it can be postulated that inhibition of TNF-a may result in otherwise benign respiratory viral infections to progress and cause significant morbidity.…”
Section: Discussionmentioning
confidence: 99%
“…На їх частку припадає 0,1-0,2 % усіх пацієнтів з ВВ і 13 % серед всіх енцефалітів встановле-ної етіології [11,26,40]. Запальні зміни в лікворі можуть бути відсутні, інколи виявляється невисокий лімфоци-тарний плеоцитоз (до 100 клітин/мкл) на фоні нормаль-ного або злегка підвищеного вмісту білка [47]. Прогноз захворювання сприятливий, одужання без залишкового неврологічного дефіциту зазвичай настає через 2-4 тижні [11, 40,41].…”
Section: (87)2017 інфекційні хворобиunclassified