T-cell non-hodgkin lymphoma in human immunodeficiency virus-1-infected individuals

1989 ◽  
Vol 31 (3) ◽  
pp. 181-187 ◽  
Author(s):  
John A. Lust ◽  
Peter M. Banks ◽  
W. Craig Hooper ◽  
Carlos V. Paya ◽  
Brian D. Kueck ◽  
...  
2020 ◽  
Vol 73 (1-2) ◽  
pp. 37-42
Author(s):  
Vanja Andric ◽  
Vesna Turkulov ◽  
Ivana Urosevic ◽  
Nebojsa Salaj ◽  
Nikola Boskovic ◽  
...  

Introduction. Even in the era of combined antiretroviral therapy, the mortality rate in patients with human immunodeficiency virus infection remains high, especially with a contributing diagnosis of a malignant disease, such as non-Hodgkin lymphoma. Given the previous, the goal of this research was to establish the incidence of non-Hodgkin lymphoma in human immunodeficiency virus positive patients, as well as to determine their clinical characteristics and mortality in regard to patients with human immunodeficiency virus only. Material and Methods. The retrospective study included 396 human immunodeficiency virus-positive patients. Medical records were reviewed to analyze the average age, duration of infection, average duration of therapy, nCD4+ T-cell count, human immunodeficiency virus viral load, as well as the number and types of malignant diseases. Results. The average age of the patients was 44.2 years; the average nCD4+ T-cell count was 296.94 cells/?L, while the mortality rate was 14.65%. The leading causes of death were non-Hodgkin lymphoma and acquired immunodeficiency syndrome. The most frequently diagnosed malignancy was non-Hodgkin lymphoma, where the average count of nCD4+ T-cells was 162.29 cells/?L. Patients with human immunodeficiency virus and non-Hodgkin lymphoma had significantly lower nCD4+ T-cell count, in regard to patients with human immunodeficiency virus only, and the mortality rate in this group of patients was 85%. Conclusion. The incidence of non-Hodgkin lymphoma in human immunodeficiency virus-positive patients represents a growing threat, given the exceptionally high mortality. The nCD4+ T-cell count may indicate acquired immunodeficiency syndrome and late diagnosis of human immunodeficiency virus together are predictors for non-Hodgkin lymphoma and its poor outcome. It points to the importance of increasing the scope of human immunodeficiency virus testing, as well as finding a better treatment approach.


Cancer ◽  
2000 ◽  
Vol 88 (7) ◽  
pp. 1696-1702 ◽  
Author(s):  
Frantz Thiessard ◽  
Philippe Morlat ◽  
Catherine Marimoutou ◽  
Eric Labouyrie ◽  
Jean-Marie Ragnaud ◽  
...  

2015 ◽  
Vol 2 (4) ◽  
Author(s):  
Sabine Kinloch-de Loes ◽  
Lucy Dorrell ◽  
Hongbing Yang ◽  
Gareth A. D. Hardy ◽  
Sabine Yerly ◽  
...  

Abstract Combination antiretroviral therapy during primary human immunodeficiency virus-1 infection may enable long-term drug-free virological control in rare individuals. We describe a female who maintained aviremia and a normal CD4+/CD8+ T cell ratio for 10 years after stopping therapy, despite a persistent viral reservoir. Cellular immune responses may have contributed to this outcome.


Blood ◽  
1991 ◽  
Vol 78 (11) ◽  
pp. 3004-3011 ◽  
Author(s):  
MJ Boyle ◽  
WA Sewell ◽  
TB Sculley ◽  
A Apolloni ◽  
JJ Turner ◽  
...  

Abstract Biopsy samples obtained from 20 patients with human immunodeficiency virus (HIV)-associated non-Hodgkin lymphoma (NHL) were assessed for evidence of Epstein-Barr virus (EBV) and HIV sequences. DNA was extracted from formalin-fixed, paraffin-embedded NHL tissue and specific viral gene sequences were sought using the polymerase chain reaction (PCR). EBV sequences were found in 10 NHL samples (50%), with five tumors showing A-type and five B-type sequences. By serologic testing, 18 of 19 patients had antibodies to EBV, with 14 patients having antibodies to A-type EBV and 11 to B-type EBV. Serology confirmed the high prevalence of type B EBV in HIV-infected patients, but was not a reliable indicator of the EBV subtype present in the lymphomas. HIV sequences were present in biopsy tissue but at a level consistent with an origin from bystander HIV-infected cells. All 20 patients were negative by enzyme-linked immunosorbent assay for antibodies to human T-cell leukemia virus-type I. The high prevalence of type B EBV in these tumors is similar to the findings in endemic Burkitt's lymphoma, where 40% of the tumors have type B viral sequences. In normal populations, type B EBV is rarely found outside the nasopharynx. These studies support the hypothesis that EBV is an important cofactor in NHL in HIV-infected persons. The finding that B- type EBV is present in 25% of HIV-associated NHL suggests that this EBV subtype may be an important human pathogen with a wider geographic distribution than originally thought.


2014 ◽  
Vol 5 (2) ◽  
pp. 179
Author(s):  
Leelavathy Budamakuntla ◽  
Eswari Loganathan ◽  
Shwetha Suryanarayan ◽  
Kumar Abhishek ◽  
Sacchidanand Sarvajnamurthy

Blood ◽  
2000 ◽  
Vol 96 (1) ◽  
pp. 242-249 ◽  
Author(s):  
Dawn R. Clark ◽  
Sjoerd Repping ◽  
Nadine G. Pakker ◽  
Jan M. Prins ◽  
Daan W. Notermans ◽  
...  

Abstract Impairment of T-cell renewal has been proposed as contributing to CD4+ T-cell depletion in persons infected with human immunodeficiency virus-1. We analyzed the T-cell development capacity of progenitors using fetal thymus organ culture. Those who progressed to AIDS had a dramatic loss in T-cell development capacity shortly after seroconversion. In contrast, long-term nonprogressors retained progenitor capacity 8 years after seroconversion. Approximately 70% of patients experienced an improvement in T-cell development capacity after receiving 6 months of potent antiretroviral therapy. Improvement in T-cell development in fetal thymus organ culture correlated with an increase in the number of naive CD4+ T cells in peripheral blood. Numbers of progenitors in blood and bone marrow after seroconversion or during therapy did not correlate with the change observed in T-cell development capacity. These data provide evidence that HIV-1 infection can interfere with T-cell renewal at the level of the progenitor cell. Interference with T-cell renewal may contribute to CD4+ T-cell depletion.


Sign in / Sign up

Export Citation Format

Share Document