Viral dynamics in human immunodeficiency virus type 1 infection

Wei, Xiping; Ghosh, Santanu; Taylor, Maria E.; Johnson, Victoria A.; Emini, Emilio A.; Deutsch, Paul; Lifson, Jeffrey D.; Bonhoeffer, Sebastian; Nowak, Martin A.; Hahn, Beatrice H.; Saag, Michael S.; Shaw, George M.

doi:10.1038/373117a0

Cited by 3,070 publications

(1,849 citation statements)

References 40 publications

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“…Following seroconversion, circulating sCD30 decreases in most cases, along with the disappearance of detectable levels of HIV antigen in the blood. Thus, during the early phases of infection, high levels of CD30 are released when a peak of viral replication, in both peripheral blood and lymph node, and high viraemia and death of CD4 + infected cells are known to occur [1][2][3].…”

Section: Discussionmentioning

confidence: 99%

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High serum level of soluble CD30 in acute primary HIV-1 infection

Pizzolo

Vinante²,

Nadali³

et al. 1997

Clinical and Experimental Immunology

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SUMMARYCD30 has been suggested to play a role in HIV infection. In this study the serum concentration of soluble CD30 (sCD30) was determined by an ELISA essay on samples collected from patients with acute primary HIV-1 infection during the acute phase (n ¼ 17) and after seroconversion (n ¼ 13). sCD30 during acute infection was consistently elevated (137·58 Ϯ 120·33 versus 6·4 Ϯ 5·4 U/ml (mean Ϯ s.d.) in normal controls; P < 0 . 0001) and decreased after seroconversion (49·1 Ϯ 66·17 U/ml; P ¼ 0 . 0018 compared with acute infection). This trend mirrored the disappearance of detectable levels of HIV antigen in the blood, resulting in a direct correlation between sCD30 and HIVAg values (P ¼ 0 . 002). These data suggest that the high levels of sCD30 observed during the peak concentration of HIVAg in acute primary HIV infection might reflect the high rate of viral replication.

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Section: Discussionmentioning

confidence: 99%

“…The highly dynamic pathogenic mechanisms involved in the earliest phase of HIV infection are complex and not yet fully elucidated [1][2][3]. Among them, a relevant role is probably played by CD30-CD30 ligand (CD30L) interactions, as suggested by several recent findings [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

High serum level of soluble CD30 in acute primary HIV-1 infection

Pizzolo

Vinante²,

Nadali³

et al. 1997

Clinical and Experimental Immunology

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“…The mechanisms by which HIV-1 kills immune cells are not completely understood. Some of these mechanisms are related to direct HIV-1-mediated cytophatic e ects, but the mean production rate of HIV-1 virions in infected individuals (1.1610 8 ± 6.8610 8 per day) cannot explain the destruction rate of lymphocytes in infected individuals (1.8610 9 ± 2610 9 per day) by direct killing (Ho et al, 1995;Wei et al, 1995). Moreover, a growing body of evidence points out that apoptosis may play an important role in AIDS pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Susceptibility of HIV-1-TAT transfected cells to undergo apoptosis. Biochemical mechanisms

Macho¹,

Calzado²,

Jiménez‐Reina³

et al. 1999

Oncogene

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The e ects of HIV-1 Tat protein on mitochondria membrane permeability and apoptosis were analysed in lymphoid cells. In this report we show that stabletransfected HIV-Tat cells are primed to undergo apoptosis upon serum withdrawal. This e ect was observed in both the Jhan T cell line and the K562 cells, the latter expressing the bcr-abl chimeric gene, which confers resistance to apoptosis induced by di erent stimuli. Using a cyto¯uorimetric approach we have determined that serum withdrawal induces a disruption of the transmembrane mitochondrial potential (Dc m ) followed by an increase of reactive oxygen species (ROS) and the subsequent DNA nuclear loss in K562-Tat cells but not in the K562-pcDNA cell line. These pre-apoptotic events were associated with the cleavage of the caspase-3, while the expression of Bcl-2, Bcl-X L and Bax proteins was not a ected by the presence of Tat. Regardless of the steady state of the Bax protein, we found that in both K562 and K562-Tat cells, this protein is located in the nucleus, but after serum withdrawal its localization was mainly in the cytoplasm. The activity of caspase-3 detected in K562-Tat cells after serum withdrawal paralleled with the mitochondria permeability transition. Nevertheless, in Jhan-Tat cells the inhibition of this caspase with the speci®c inhibitor, z-DEVD-cmk, did not a ect the disruption of the mitochondria potential induced by serum withdrawal. Interestingly, we found that HIV-Tat protein accumulates at the mitochondria in the K562-Tat cells cultured under low serum conditions, and this mitochondrial localization correlated with the Dc m disruption detected in these cells. In addition, HIV-1 Tat protein synergies with protoporphyrin IX (PPIX), a ligand of the mitochondrial benzodiazepine receptor, in the induction of apoptosis in both Jhan and K562 cells. Thus, HIV-1 Tat protein may induce apoptosis by a mechanism that involves mitochondrial PT and may contribute to the lymphocyte depletion seen in AIDS patients.

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“…The host's immune response usually kicks in after a few weeks and the level of virus in the blood declines to bring HIV-1 infection into its second phase. Viral replication is still active and cells are rapidly being infected and eliminated during this period [35,36]. The turnover of T-cells gradually leads to a decline in their number [37].…”

Section: Targets Cells Of Hiv-1mentioning

confidence: 99%