Viral burden and disease progression in HIV-1-infected patients with sickle cell anemia

Omar Bagasra, Robert M. Steiner, Samir K. Ballas, Oswaldo Castro, Geethanjali Dornadula, Stephen Embury, Donald Jungkind, Lisa Bobroski, Abdullah Kutlar, Sandra Burchott

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The spleen and lymph nodes are major sites of human immunodeficiency virus type 1 (HIV-1) replication, mutation, and genetic variation in vivo. If a major portion of the lymphatic tissue, such as the spleen, is removed or otherwise is unavailable for invasion by the HIV-1 virus, will the course of the infection be altered, resulting in a prolonged symptom-free interval or even increased survival? The spleen of most adults with sickle cell anemia (SS) is nonfunctional due to recurrent episodes of microinfarction. If autosplenectomized SS patients are exposed to HIV-1, they may be ideal candidates to examine the question of whether absence of splenic function at the time of infection will positively alter the course of HIV-1-related disease. All SS patients with a diagnosis of HIV-1 infection at five university sickle cell centers were included in the patient cohort. Patients in active treatment or in follow-up (group A, n = 11) underwent a series of quantitative viral studies to determine their HIV-1 viral burden. The studies included the branched-DNA signal amplification assay, quantitative DNA- polymerase chain reaction (PCR), quantitative reverse transcription (RT)- initiated-PCR, and in situ PCR. All patients who died of the complications of the acquired immunodeficiency syndrome (AIDS) or of SS, lost to follow-up, or were otherwise unavailable for study (Group B: n = 7) were included in the total patient group. None of the patients in group B underwent quantitative viral studies. In addition, a control population (group C, n = 36) of HIV-1- infected African Americans without SS, of similar age and gender to the SS patients, were compared with the study population for outcomes. In eight of 11 active patients (group A), the CD4+ T-lymphocyte counts were normal and viral burdens were low for an average of 10.25 years following diagnosis. These eight patients all from group A were the only long-term nonprogressors (44%) among a total of 18 SS patients (groups A and B). In group C (control), only five patients of 36 were long-term nonprogressors (13.9%). Five patients (28%) of the total SS group (groups A and B) succumbed to AIDS. One of the five was from Group A. The evaluation of a limited number of adult individuals suggests that a significant proportion of HIV-1-seropositive SS patients (44%) may be asymptomatic long-term nonprogressors. In these patients, the CD4+ T-lymphocyte counts remained high and theft viral burdens were remarkably lower than in non-SS HIV-1-seropositive individuals. Whereas this study does not prove an 'autosplenectomy' hypothesis, it suggests that in patients with both SS and HIV-1 infection, the retroviral disease may be ameliorated by host factors of which absence of splenic function prior to HIV-1 infection may be one.

Original languageEnglish (US)
Pages (from-to)199-207
Number of pages9
JournalAmerican Journal of Hematology
Volume59
Issue number3
DOIs
StatePublished - Nov 1 1998

Fingerprint

Sickle Cell Anemia
Virus Diseases
Viral Load
Disease Progression
HIV-1
Spleen
CD4 Lymphocyte Count
Polymerase Chain Reaction
Acquired Immunodeficiency Syndrome
Branched DNA Signal Amplification Assay
Theft
T-Lymphocytes
Control Groups
Lost to Follow-Up
Lymphoid Tissue
DNA-Directed DNA Polymerase
Virus Replication
Infection
Population Groups
African Americans

Keywords

  • Anemia
  • DNA
  • HIV-1 sickle cell
  • RNA

ASJC Scopus subject areas

  • Hematology

Cite this

Viral burden and disease progression in HIV-1-infected patients with sickle cell anemia. / Bagasra, Omar; Steiner, Robert M.; Ballas, Samir K.; Castro, Oswaldo; Dornadula, Geethanjali; Embury, Stephen; Jungkind, Donald; Bobroski, Lisa; Kutlar, Abdullah; Burchott, Sandra.

In: American Journal of Hematology, Vol. 59, No. 3, 01.11.1998, p. 199-207.

Research output: Contribution to journalArticle

Bagasra, O, Steiner, RM, Ballas, SK, Castro, O, Dornadula, G, Embury, S, Jungkind, D, Bobroski, L, Kutlar, A & Burchott, S 1998, 'Viral burden and disease progression in HIV-1-infected patients with sickle cell anemia', American Journal of Hematology, vol. 59, no. 3, pp. 199-207. https://doi.org/10.1002/(SICI)1096-8652(199811)59:3<199::AID-AJH4>3.0.CO;2-L
Bagasra, Omar ; Steiner, Robert M. ; Ballas, Samir K. ; Castro, Oswaldo ; Dornadula, Geethanjali ; Embury, Stephen ; Jungkind, Donald ; Bobroski, Lisa ; Kutlar, Abdullah ; Burchott, Sandra. / Viral burden and disease progression in HIV-1-infected patients with sickle cell anemia. In: American Journal of Hematology. 1998 ; Vol. 59, No. 3. pp. 199-207.
@article{4122498ca85041858756d839bbdce4ec,
title = "Viral burden and disease progression in HIV-1-infected patients with sickle cell anemia",
abstract = "The spleen and lymph nodes are major sites of human immunodeficiency virus type 1 (HIV-1) replication, mutation, and genetic variation in vivo. If a major portion of the lymphatic tissue, such as the spleen, is removed or otherwise is unavailable for invasion by the HIV-1 virus, will the course of the infection be altered, resulting in a prolonged symptom-free interval or even increased survival? The spleen of most adults with sickle cell anemia (SS) is nonfunctional due to recurrent episodes of microinfarction. If autosplenectomized SS patients are exposed to HIV-1, they may be ideal candidates to examine the question of whether absence of splenic function at the time of infection will positively alter the course of HIV-1-related disease. All SS patients with a diagnosis of HIV-1 infection at five university sickle cell centers were included in the patient cohort. Patients in active treatment or in follow-up (group A, n = 11) underwent a series of quantitative viral studies to determine their HIV-1 viral burden. The studies included the branched-DNA signal amplification assay, quantitative DNA- polymerase chain reaction (PCR), quantitative reverse transcription (RT)- initiated-PCR, and in situ PCR. All patients who died of the complications of the acquired immunodeficiency syndrome (AIDS) or of SS, lost to follow-up, or were otherwise unavailable for study (Group B: n = 7) were included in the total patient group. None of the patients in group B underwent quantitative viral studies. In addition, a control population (group C, n = 36) of HIV-1- infected African Americans without SS, of similar age and gender to the SS patients, were compared with the study population for outcomes. In eight of 11 active patients (group A), the CD4+ T-lymphocyte counts were normal and viral burdens were low for an average of 10.25 years following diagnosis. These eight patients all from group A were the only long-term nonprogressors (44{\%}) among a total of 18 SS patients (groups A and B). In group C (control), only five patients of 36 were long-term nonprogressors (13.9{\%}). Five patients (28{\%}) of the total SS group (groups A and B) succumbed to AIDS. One of the five was from Group A. The evaluation of a limited number of adult individuals suggests that a significant proportion of HIV-1-seropositive SS patients (44{\%}) may be asymptomatic long-term nonprogressors. In these patients, the CD4+ T-lymphocyte counts remained high and theft viral burdens were remarkably lower than in non-SS HIV-1-seropositive individuals. Whereas this study does not prove an 'autosplenectomy' hypothesis, it suggests that in patients with both SS and HIV-1 infection, the retroviral disease may be ameliorated by host factors of which absence of splenic function prior to HIV-1 infection may be one.",
keywords = "Anemia, DNA, HIV-1 sickle cell, RNA",
author = "Omar Bagasra and Steiner, {Robert M.} and Ballas, {Samir K.} and Oswaldo Castro and Geethanjali Dornadula and Stephen Embury and Donald Jungkind and Lisa Bobroski and Abdullah Kutlar and Sandra Burchott",
year = "1998",
month = "11",
day = "1",
doi = "10.1002/(SICI)1096-8652(199811)59:3<199::AID-AJH4>3.0.CO;2-L",
language = "English (US)",
volume = "59",
pages = "199--207",
journal = "American Journal of Hematology",
issn = "0361-8609",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - Viral burden and disease progression in HIV-1-infected patients with sickle cell anemia

AU - Bagasra, Omar

AU - Steiner, Robert M.

AU - Ballas, Samir K.

AU - Castro, Oswaldo

AU - Dornadula, Geethanjali

AU - Embury, Stephen

AU - Jungkind, Donald

AU - Bobroski, Lisa

AU - Kutlar, Abdullah

AU - Burchott, Sandra

PY - 1998/11/1

Y1 - 1998/11/1

N2 - The spleen and lymph nodes are major sites of human immunodeficiency virus type 1 (HIV-1) replication, mutation, and genetic variation in vivo. If a major portion of the lymphatic tissue, such as the spleen, is removed or otherwise is unavailable for invasion by the HIV-1 virus, will the course of the infection be altered, resulting in a prolonged symptom-free interval or even increased survival? The spleen of most adults with sickle cell anemia (SS) is nonfunctional due to recurrent episodes of microinfarction. If autosplenectomized SS patients are exposed to HIV-1, they may be ideal candidates to examine the question of whether absence of splenic function at the time of infection will positively alter the course of HIV-1-related disease. All SS patients with a diagnosis of HIV-1 infection at five university sickle cell centers were included in the patient cohort. Patients in active treatment or in follow-up (group A, n = 11) underwent a series of quantitative viral studies to determine their HIV-1 viral burden. The studies included the branched-DNA signal amplification assay, quantitative DNA- polymerase chain reaction (PCR), quantitative reverse transcription (RT)- initiated-PCR, and in situ PCR. All patients who died of the complications of the acquired immunodeficiency syndrome (AIDS) or of SS, lost to follow-up, or were otherwise unavailable for study (Group B: n = 7) were included in the total patient group. None of the patients in group B underwent quantitative viral studies. In addition, a control population (group C, n = 36) of HIV-1- infected African Americans without SS, of similar age and gender to the SS patients, were compared with the study population for outcomes. In eight of 11 active patients (group A), the CD4+ T-lymphocyte counts were normal and viral burdens were low for an average of 10.25 years following diagnosis. These eight patients all from group A were the only long-term nonprogressors (44%) among a total of 18 SS patients (groups A and B). In group C (control), only five patients of 36 were long-term nonprogressors (13.9%). Five patients (28%) of the total SS group (groups A and B) succumbed to AIDS. One of the five was from Group A. The evaluation of a limited number of adult individuals suggests that a significant proportion of HIV-1-seropositive SS patients (44%) may be asymptomatic long-term nonprogressors. In these patients, the CD4+ T-lymphocyte counts remained high and theft viral burdens were remarkably lower than in non-SS HIV-1-seropositive individuals. Whereas this study does not prove an 'autosplenectomy' hypothesis, it suggests that in patients with both SS and HIV-1 infection, the retroviral disease may be ameliorated by host factors of which absence of splenic function prior to HIV-1 infection may be one.

AB - The spleen and lymph nodes are major sites of human immunodeficiency virus type 1 (HIV-1) replication, mutation, and genetic variation in vivo. If a major portion of the lymphatic tissue, such as the spleen, is removed or otherwise is unavailable for invasion by the HIV-1 virus, will the course of the infection be altered, resulting in a prolonged symptom-free interval or even increased survival? The spleen of most adults with sickle cell anemia (SS) is nonfunctional due to recurrent episodes of microinfarction. If autosplenectomized SS patients are exposed to HIV-1, they may be ideal candidates to examine the question of whether absence of splenic function at the time of infection will positively alter the course of HIV-1-related disease. All SS patients with a diagnosis of HIV-1 infection at five university sickle cell centers were included in the patient cohort. Patients in active treatment or in follow-up (group A, n = 11) underwent a series of quantitative viral studies to determine their HIV-1 viral burden. The studies included the branched-DNA signal amplification assay, quantitative DNA- polymerase chain reaction (PCR), quantitative reverse transcription (RT)- initiated-PCR, and in situ PCR. All patients who died of the complications of the acquired immunodeficiency syndrome (AIDS) or of SS, lost to follow-up, or were otherwise unavailable for study (Group B: n = 7) were included in the total patient group. None of the patients in group B underwent quantitative viral studies. In addition, a control population (group C, n = 36) of HIV-1- infected African Americans without SS, of similar age and gender to the SS patients, were compared with the study population for outcomes. In eight of 11 active patients (group A), the CD4+ T-lymphocyte counts were normal and viral burdens were low for an average of 10.25 years following diagnosis. These eight patients all from group A were the only long-term nonprogressors (44%) among a total of 18 SS patients (groups A and B). In group C (control), only five patients of 36 were long-term nonprogressors (13.9%). Five patients (28%) of the total SS group (groups A and B) succumbed to AIDS. One of the five was from Group A. The evaluation of a limited number of adult individuals suggests that a significant proportion of HIV-1-seropositive SS patients (44%) may be asymptomatic long-term nonprogressors. In these patients, the CD4+ T-lymphocyte counts remained high and theft viral burdens were remarkably lower than in non-SS HIV-1-seropositive individuals. Whereas this study does not prove an 'autosplenectomy' hypothesis, it suggests that in patients with both SS and HIV-1 infection, the retroviral disease may be ameliorated by host factors of which absence of splenic function prior to HIV-1 infection may be one.

KW - Anemia

KW - DNA

KW - HIV-1 sickle cell

KW - RNA

UR - http://www.scopus.com/inward/record.url?scp=0031792483&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031792483&partnerID=8YFLogxK

U2 - 10.1002/(SICI)1096-8652(199811)59:3<199::AID-AJH4>3.0.CO;2-L

DO - 10.1002/(SICI)1096-8652(199811)59:3<199::AID-AJH4>3.0.CO;2-L

M3 - Article

C2 - 9798657

AN - SCOPUS:0031792483

VL - 59

SP - 199

EP - 207

JO - American Journal of Hematology

JF - American Journal of Hematology

SN - 0361-8609

IS - 3

ER -