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.
Lymphoid Interstitial Pneumonia: A Narrative Review
Swigris et al.
Chest 2002;122:2150-2164.
ABSTRACT
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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
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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.
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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.
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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.
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Differential Effects of Interleukin-13 on Cytomegalovirus and Human Immunodeficiency Virus Infection in Human Alveolar Macrophages
Hatch et al.
Blood 1997;89:3443-3450.
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