scholarly journals Role of dendritic cells infected with human herpesvirus 6 in virus transmission to CD4+ T cells

Virology ◽  
2009 ◽  
Vol 385 (2) ◽  
pp. 294-302 ◽  
Author(s):  
Masaya Takemoto ◽  
Takayoshi Imasawa ◽  
Koichi Yamanishi ◽  
Yasuko Mori
2006 ◽  
Vol 50 (10) ◽  
pp. 787-803 ◽  
Author(s):  
Fang Wang ◽  
Kun Yao ◽  
Quan-Zhang Yin ◽  
Feng Zhou ◽  
Chuan-Lin Ding ◽  
...  

1994 ◽  
Vol 68 (8) ◽  
pp. 5326-5329 ◽  
Author(s):  
H Hasegawa ◽  
Y Utsunomiya ◽  
M Yasukawa ◽  
K Yanagisawa ◽  
S Fujita

Blood ◽  
1995 ◽  
Vol 85 (5) ◽  
pp. 1263-1271 ◽  
Author(s):  
L Flamand ◽  
J Gosselin ◽  
I Stefanescu ◽  
D Ablashi ◽  
J Menezes

Human herpesvirus-6 (HHV-6), the etiologic agent of roseola, is ubiquitous, establishes latency in the host, and can infect a variety of immunocompetent cells, with CD4+ T lymphocytes being the targets in which it replicates most efficiently. The present study was undertaken to learn more about specific immunobiologic effects of HHV-6 infection on T-lymphocyte functions. Our data demonstrate that infection of peripheral blood mononuclear cells (PBMC) by HHV-6 results in suppression of T-lymphocyte functions, as evidenced by reduced interleukin-2 (IL-2) synthesis and cellular proliferation. In fact, HHV- 6-infected PBMC secreted 50% less IL-2 than mock-infected cells after mitogenic stimulation with OKT3 antibody or phytohemmaglutinin (PHA). The inhibition of IL-2 by HHV-6 was also observed in enriched T-cell cultures, suggesting a direct effect of this virus on this cell type. Messenger RNA (mRNA) analysis by reverse-transcriptase polymerase chain reaction (PCR) indicated that HHV-6 diminishes IL-2 mRNA levels in mitogen-stimulated peripheral blood T cells. These results were also confirmed by Northern blot using the leukemic T-cell line Jurkat. This inhibitory effect of HHV-6 did not require infectious virus, as the use of UV-irradiated HHV-6 produced similar results. Moreover, HHV-6- infected PBMC showed up to an 85% reduction in their mitogen-driven proliferative response, as compared with sham-infected cells. Proliferation of both CD4+ and CD8+ T cells was affected by HHV-6. Taken together, our data show that infection of T cells by HHV-6 results in immune suppression characterized by a downregulation of IL-2 mRNA and protein synthesis accompanied by diminished cellular proliferation.


2020 ◽  
Vol 346 ◽  
pp. 577313 ◽  
Author(s):  
Hossein Keyvani ◽  
Hamid Zahednasab ◽  
Hussain ali abraham Aljanabi ◽  
Muhammad Asadi ◽  
Rasoul Mirzaei ◽  
...  

Blood ◽  
1999 ◽  
Vol 94 (5) ◽  
pp. 1545-1549 ◽  
Author(s):  
Masanori Daibata ◽  
Takahiro Taguchi ◽  
Yuiko Nemoto ◽  
Hirokuni Taguchi ◽  
Isao Miyoshi

Abstract Human herpesvirus 6 (HHV-6) genome has been detected in several human lymphoproliferative disorders with no signs of active viral infection, and found to be integrated into chromosomes in some cases. We previously reported a woman with HHV-6–infected Burkitt’s lymphoma. Fluorescence in situ hybridization showed that the viral genome was integrated into the long arm of chromosome 22 (22q13). The patient’s asymptomatic husband also carried HHV-6 DNA integrated at chromosome locus 1q44. To assess the possibility of chromosomal transmission of HHV-6 DNA, we looked for HHV-6 DNA in the peripheral blood of their daughter. She had HHV-6 DNA on both chromosomes 22q13 and 1q44, identical to the site of viral integration of her mother and father, respectively. The findings suggested that her viral genomes were inherited chromosomally from both parents. The 3 family members were all seropositive for HHV-6, but showed no serological signs of active infection. To confirm the presence of HHV-6 DNA sequences, we performed polymerase chain reaction (PCR) with 7 distinct primer pairs that target different regions of HHV-6. The viral sequences were consistently detected by single-step PCR in all 3 family members. We propose a novel latent form for HHV-6, in which integrated viral genome can be chromosomally transmitted. The possible role of the chromosomally integrated HHV-6 in the pathogenesis of lymphoproliferative diseases remains to be explained.


1992 ◽  
Vol 8 (12) ◽  
pp. 2031-2037 ◽  
Author(s):  
M. CIRONE ◽  
C. ZOMPETTA ◽  
A. ANGELONI ◽  
D.V. ABLASHI ◽  
S.Z. SALAHUDDIN ◽  
...  

2004 ◽  
Vol 200 (10) ◽  
pp. 1279-1288 ◽  
Author(s):  
Jean-François Arrighi ◽  
Marjorie Pion ◽  
Eduardo Garcia ◽  
Jean-Michel Escola ◽  
Yvette van Kooyk ◽  
...  

Dendritic cells (DCs) are essential for the early events of human immunodeficiency virus (HIV) infection. Model systems of HIV sexual transmission have shown that DCs expressing the DC-specific C-type lectin DC-SIGN capture and internalize HIV at mucosal surfaces and efficiently transfer HIV to CD4+ T cells in lymph nodes, where viral replication occurs. Upon DC–T cell clustering, internalized HIV accumulates on the DC side at the contact zone (infectious synapse), between DCs and T cells, whereas HIV receptors and coreceptors are enriched on the T cell side. Viral concentration at the infectious synapse may explain, at least in part, why DC transmission of HIV to T cells is so efficient. Here, we have investigated the role of DC-SIGN on primary DCs in X4 HIV-1 capture and transmission using small interfering RNA–expressing lentiviral vectors to specifically knockdown DC-SIGN. We demonstrate that DC-SIGN− DCs internalize X4 HIV-1 as well as DC-SIGN+ DCs, although binding of virions is reduced. Strikingly, DC-SIGN knockdown in DCs selectively impairs infectious synapse formation between DCs and resting CD4+ T cells, but does not prevent the formation of DC–T cells conjugates. Our results demonstrate that DC-SIGN is required downstream from viral capture for the formation of the infectious synapse between DCs and T cells. These findings provide a novel explanation for the role of DC-SIGN in the transfer and enhancement of HIV infection from DCs to T cells, a crucial step for HIV transmission and pathogenesis.


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