You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT JAMA
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 256 No. 17, November 7, 1986 TABLE OF CONTENTS
  JAMA
  •  Online Features
  ARTICLE
 This Article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Contact me when this article is cited
 Related Content
 •Similar articles in JAMA

Detection of HTLV-III RNA in lungs of patients with AIDS and pulmonary involvement

K. J. Chayt, M. E. Harper, L. M. Marselle, E. B. Lewin, R. M. Rose, J. M. Oleske, L. G. Epstein, F. Wong-Staal and R. C. Gallo

A majority of pediatric patients and rare adult patients with the acquired immunodeficiency syndrome (AIDS) develop a chronic respiratory disorder referred to as "lymphocytic interstitial pneumonitis" (LIP). Efforts to identify an infectious agent responsible for this process so far have failed. In this study, frozen sections of lungs from patients with AIDS and pulmonary disease were tested by in situ molecular hybridization for the presence of cells infected with human T-cell lymphotropic virus type III (HTLV-III) and expressing viral RNA. In the case of an infant with LIP, a relatively high frequency (0.1%) of cells in the lung were found to be positive for HTLV-III RNA. This number is the lower limit of total cells infected since the in situ hybridization technique as applied in this study depends on expression of HTLV-III genes, and previous evidence indicates that a proportion of cells infected with HTLV-III may not express viral RNA. Moreover, this degree of infection of the lung is likely limited to LIP, since in ten patients with AIDS and pulmonary diseases other than LIP, only 0% to 0.002% of cells in lung were positive for viral RNA expression. Thus, HTLV-III may play a direct causal role in the development of LIP in infected patients, implicating its involvement in yet another of the diverse clinical diseases associated with this virus.

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Lymphoid Interstitial Pneumonia: A Narrative Review
Swigris et al.
Chest 2002;122:2150-2164.
ABSTRACT | FULL TEXT  

Endothelial Cells Enhance Human Immunodeficiency Virus Type 1 Replication in Macrophages through a C/EBP-Dependent Mechanism
Lee et al.
J. Virol. 2001;75:9703-9712.
ABSTRACT | FULL TEXT  

Patterns of Chemokine Receptor Fusion Cofactor Utilization by Human Immunodeficiency Virus Type 1 Variants from the Lungs and Blood
Singh et al.
J. Virol. 1999;73:6680-6690.
ABSTRACT | FULL TEXT  

Lymphocytic Alveolitis, Bronchoalveolar Lavage Viral Load, and Outcome in Human Immunodeficiency Virus Infection
TWIGG et al.
Am. J. Respir. Crit. Care Med. 1999;159:1439-1444.
ABSTRACT | FULL TEXT  

Differential Tropism and Chemokine Receptor Expression of Human Immunodeficiency Virus Type 1 in Neonatal Monocytes, Monocyte-Derived Macrophages, and Placental Macrophages
Fear et al.
J. Virol. 1998;72:1334-1344.
ABSTRACT | FULL TEXT  

Differential Effects of Interleukin-13 on Cytomegalovirus and Human Immunodeficiency Virus Infection in Human Alveolar Macrophages
Hatch et al.
Blood 1997;89:3443-3450.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1986 American Medical Association. All Rights Reserved.