Subject:
AIDS
From:
"" <rossip>
Date: 09-Dec-97
Name: T10350_8a002Xi
Database: Medline <1981 to 1986>
Set Search
Results
--------------------------------------------------------------------------001 exp hiv/
340
002 exp acquired immunodeficiency syndrome/
5950
003 1 and 2
213
004 from 3 keep 3-4,7,14,28,50,64-65,94,103,109,127,156,169,176,
18
<1>
Unique Identifier
87156949
Authors
Volsky DJ. Sakai K. Stevenson M. Dewhurst S.
Title
Retroviral etiology of the acquired immune deficiency syndrome (AIDS).
[Review] [78 refs]
Source
AIDS Research. 2 Suppl 1:S35-48, 1986 Dec.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/et [Etiology]
Acquired Immunodeficiency Syndrome/mi [Microbiology]
DNA, Viral/an [Analysis]
Genes, Viral
Human
HIV/cl [Classification]
HIV/ge [Genetics]
HIV/ip [Isolation & Purification]
*HIV/py [Pathogenicity]
*HTLV-BLV Viruses/cl [Classification]
HTLV-BLV Viruses/ge [Genetics]
Polymorphism, Restriction Fragment Length
Support, U.S. Gov't, P.H.S.
Variation (Genetics)
Abstract
The acquired immune deficiency syndrome (AIDS) is characterized by severe
immunological defects resulting in opportunistic infections and
malignancies. A novel human retrovirus, known under the terms of LAV,
HTLV-III, ARV or as a human immunodeficiency virus (HIV), has been defined
as the infectious agent responsible for the induction of the immunologic
disorders in AIDS. However, two recent lines of evidence, reviewed in this
article, complicate the etiological picture of AIDS: the HIV family
appears to consist of a great number of diverse, and perhaps diversifying
in vivo, members that exhibit different molecular and biological
properties; the human retrovirus family may contain yet another distinct
class of member viruses that resemble HIV morphologically and structurally
but may differ in their pathogenicity. Our understanding of the retroviral
etiology of AIDS may be far from complete. [References: 78]
Registry Numbers
0 (DNA, Viral).
<2>
Unique Identifier
87156930
Authors
Purtilo DT.
Title
Lymphotropic viruses, Epstein-Barr virus (EBV) and human T-cell
lymphotropic virus-I (HTLV-I)/adult T-cell leukemia virus (ATLV), and
HTLV-III/human immune deficiency virus (HIV) as etiological agents of
malignant lymphoma and immune deficiency. [Review] [39 refs]
Source
AIDS Research. 2 Suppl 1:S1-6, 1986 Dec.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/et [Etiology]
B-Lymphocytes/im [Immunology]
B-Lymphocytes/mi [Microbiology]
Comparative Study
*Herpesvirus 4, Human/py [Pathogenicity]
Human
HIV/py [Pathogenicity]
*HTLV-BLV Infections/co [Complications]
HTLV-BLV Infections/im [Immunology]
*HTLV-BLV Viruses/py [Pathogenicity]
Immune Tolerance
Immunologic Surveillance
*Lymphoma/et [Etiology]
T-Lymphocytes/im [Immunology]
T-Lymphocytes/mi [Microbiology]
*Tumor Virus Infections/co [Complications]
Tumor Virus Infections/im [Immunology]
Abstract
The ubiquitous, DNA herpesvirus, EBV, has B cell tropism and the
geographically restricted RNA retrovirus, ATLV/HTLV-I has T cell tropism.
Clinical descriptions by Burkitt and Takatsuki led to discovery of these
viruses which infect silently early in life; however, ATLV is also
transmitted to a spouse or by blood transfusion. In normal seropositive
persons both viruses infect only 1 in about 10,000 B or T cells,
respectively. EBV is associated with Burkitt's lymphoma, nasopharyngeal
carcinoma, and infectious mononucleosis. ATLV is associated with adult T
cell leukemia/lymphoma and smoldering T cell lymphoma. EBV infects
polyclonally and is controlled by multiple cellular and humoral control
mechanisms. Escape from immune surveillance as in immune deficient African
children with malaria, males with x-linked lymphoproliferative syndrome,
organ transplant recipients, and AIDS patients permits conversion from
polyclonal to oligoclonal and finally, monoclonal malignancy. T cell
immune defects permit proliferation of cells which undergo molecular
and/or cytogenetic alterations. In contrast to EBV, which is integrated
and nonintegrated in B cells, ATLV is monoclonally integrated. Viral
transforming proteins and immune suppressive substances are produced.
Immune deficiency in silent carriers of ATLV and in those with smoldering
ATL suggest that immune surveillance deters emergence of ATL. Prevention
of primary infection by vaccination against these lymphotropic viruses,
and use of immunotherapy and antiviral drugs may potentially retard
conversion of infected B or T cells to monoclonal malignancy. [References:
39]
<3>
Unique Identifier
87062962
Authors
Allain JP. Laurian Y. Paul DA. Senn D.
Title
Serological markers in early stages of human immunodeficiency virus
infection in haemophiliacs.
Source
Lancet. 2(8518):1233-6, 1986 Nov 29.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/di [Diagnosis]
Adolescence
Adult
Antibodies, Viral/an [Analysis]
Antigens, Viral/an [Analysis]
Child
Comparative Study
Enzyme-Linked Immunosorbent Assay
*Hemophilia/co [Complications]
Human
HIV/im [Immunology]
Immunoenzyme Techniques
Support, Non-U.S. Gov't
Time Factors
Viral Core Proteins/im [Immunology]
Viral Envelope Proteins/im [Immunology]
Abstract
Immunoassays for human immunodeficiency virus antigen (HIV Ag) and for
antibody to HIV core and envelope (CIA-RA) were done on serial specimens
from 40 haemophiliacs who had become seropositive on screening by
enzyme-linked immunosorbent assay (ELISA). HIV Ag was detectable in 9
subjects and antibodies to envelope in 11 subjects before ELISA
seroconversion. The apparent sequence of markers is HIV Ag, antibody to
envelope, then antibody to core. Antigenaemia could be detected as soon as
2 weeks after infection and lasted 3-5 months. 82% agreement was seen
between CIA-RA and western blot; CIA was more sensitive to envelope
antibody and western blot was more sensitive to core antibody.
Registry Numbers
0 (Antibodies, Viral). 0 (Antigens, Viral). 0 (Viral Core Proteins). 0
(Viral Envelope Proteins).
<4>
Unique Identifier
87013527
Authors
Mann JM. Bila K. Colebunders RL. Kalemba K. Khonde N. Bosenge N.
Nzilambi N. Malonga M. Jansegers L. Francis H. et al.
Title
Natural history of human immunodeficiency virus infection in Zaire.
Source
Lancet. 2(8509):707-9, 1986 Sep 27.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/im [Immunology]
*Acquired Immunodeficiency Syndrome/pp [Physiopathology]
Antibodies, Viral/an [Analysis]
Female
Follow-Up Studies
Human
HIV/im [Immunology]
Male
Zaire
Abstract
The natural history of human immunodeficiency virus (HIV) infection in
Zaire was determined by identifying in October, 1984, 125 seropositive
hospital personnel without signs or symptoms and 145 age and sex matched
seronegative controls from the same population. Between July, 1985, and
February, 1986, 67 seropositives, including 38 men and 29 women, and 113
seronegatives were interviewed and examined by an observer who did not
know their serological status. The acquired immunodeficiency syndrome
(AIDS) had developed in 1 seropositive and no seronegatives (rate
difference, 1.3/100 person-years [py]; 95% confidence interval 0-3.3/100
py); AIDS-related complex or generalised lymphadenopathy had developed in
8 seropositives (12%) and 1 seronegative (1%) (rate ratio, 13.2; 95%
confidence interval 1.3-134.6); and minimal lymphadenopathy had developed
in 19 seropositives (28%) and 8 seronegatives (7%) (rate ratio, 3.9; 95%
confidence interval 1.8-8.4). These data provide the first estimates for
rates of progression to AIDS or AIDS-related conditions among healthy HIV
seropositive heterosexual adults. Rates observed in this study are similar
to those reported in US or European homosexual or bisexual men.
Registry Numbers
0 (Antibodies, Viral).
<5>
Unique Identifier
87144860
Authors
Blijham GH.
Title
The pathogenesis of the acquired immunodeficiency syndrome. [Review] [63
refs]
Source
Netherlands Journal of Medicine. 29(12):420-6, 1986.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/im [Immunology]
*Acquired Immunodeficiency Syndrome/pp [Physiopathology]
Human
HIV/im [Immunology]
T-Lymphocytes, Helper-Inducer/im [Immunology]
<6>
Unique Identifier
87101905
Authors
Lange JM. Paul DA. Huisman HG. de Wolf F. van den Berg H. Coutinho
RA. Danner SA. van der Noordaa J. Goudsmit J.
Title
Persistent HIV antigenaemia and decline of HIV core antibodies associated
with transition to AIDS.
Source
British Medical Journal Clinical Research Ed.. 293(6560):1459-62, 1986
Dec 6.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/im [Immunology]
Adult
*Antibodies, Viral/an [Analysis]
*Antigens, Viral/an [Analysis]
Blood Transfusion
Child, Preschool
Homosexuality
Human
*HIV/im [Immunology]
IgG/an [Analysis]
Infant
Male
Support, Non-U.S. Gov't
Time Factors
Viral Core Proteins/im [Immunology]
Abstract
Sequential serum samples from 13 homosexual men who seroconverted for
antibodies to human immunodeficiency virus (HIV) were tested for HIV
antigen. In one of these men, who developed the acquired immune deficiency
syndrome (AIDS), HIV antigenaemia preceded the onset of AIDS by more than
a year and persisted throughout the course of the disease. This
antigenaemia was accompanied by the disappearance of IgG antibody
reactivity to the major HIV core protein p24. In none of the 12 others,
who all remained without serious disease, were serum concentrations of HIV
antigen detected, except on one occasion in one man. All their serum
samples showed strong IgG antibody reactivity to p24. Nine children who
were infected with HIV in 1981 by plasma transfusion from a single donor
were also followed up for HIV antigenaemia. HIV antigen was almost
constantly present in the serum (26 of 28 samples) of five children who
developed AIDS related complex or AIDS and less often in the serum (four
of 10 samples) of four children who remained free of symptoms. The two
children who developed AIDS showed a virtual absence of antibody
reactivity to p24. These results indicate that increased HIV gene
expression is a contributing factor to the development of AIDS and also
provide evidence for a switch from latent to active HIV infection.
Registry Numbers
0 (Antibodies, Viral). 0 (Antigens, Viral). 0 (HIV Antibodies). 0 (HIV
Antigens). 0 (Viral Core Proteins).
<7>
Unique Identifier
87069956
Authors
Walker CM. Moody DJ. Stites DP. Levy JA.
Title
CD8+ lymphocytes can control HIV infection in vitro by suppressing virus
replication.
Source
Science. 234(4783):1563-6, 1986 Dec 19.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/im [Immunology]
Acquired Immunodeficiency Syndrome/th [Therapy]
Antigens, Surface
Cells, Cultured
Human
HIV/im [Immunology]
*HIV/ph [Physiology]
Male
RNA-Directed DNA Polymerase/me [Metabolism]
Support, Non-U.S. Gov't
*T-Lymphocytes/im [Immunology]
*Virus Replication
Abstract
Lymphocytes bearing the CD8 marker were shown to suppress replication of
human immunodeficiency virus (HIV) in peripheral blood mononuclear cells.
The effect was dose-dependent and most apparent with autologous
lymphocytes; it did not appear to be mediated by a cytotoxic response.
This suppression of HIV replication could be demonstrated by the addition
of CD8+ cells at the initiation of virus production as well as after
several weeks of virus replication by cultured cells. The observations
suggest a potential approach to therapy in which autologous CD8
lymphocytes could be administered to individuals to inhibit HIV
replication and perhaps progression of disease.
Registry Numbers
EC 2-7-7-49 (RNA-Directed DNA Polymerase). 0 (Antigens, Surface).
<8>
Unique Identifier
87065140
Authors
Weiss RA. Clapham PR. Weber JN. Dalgleish AG. Lasky LA. Berman PW.
Title
Variable and conserved neutralization antigens of human immunodeficiency
virus.
Source
Nature. 324(6097):572-5, 1986 Dec 11-17.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/im [Immunology]
Animal
Antibodies, Viral/im [Immunology]
*Antigens, Viral/im [Immunology]
Complement/im [Immunology]
Cross Reactions
Epitopes/im [Immunology]
Guinea Pigs
Human
*HIV/im [Immunology]
Neutralization Tests
Rabbits
Recombinant Proteins/im [Immunology]
Support, Non-U.S. Gov't
Viral Envelope Proteins/im [Immunology]
Abstract
Human immunodeficiency virus type 1 (HIV-1, HTLV-III/LAV), the retrovirus
responsible for acquired immune deficiency syndrome (AIDS), shows a high
degree of genetic polymorphism, particularly in the env gene. We have
examined sera from rabbits and guinea pigs immunized with gp130, a
recombinant env glycoprotein, and sera from HIV-1-infected subjects, to
test their capacity to neutralize a panel of genetically divergent HIV-1
isolates. The sera raised against recombinant antigen specifically
neutralized the virus strain from which the env gene was cloned
(HTLV-IIIB), but not an independent isolate (HTLV-IIIRF). One rabbit serum
tested on seven isolates cross-neutralized two at lower titres. In
contrast, human sera from Britain and Uganda, chosen for ability to
neutralize HTLV-IIIRF, cross-neutralized six other HIV-1 isolates. When
serum and isolate were derived from the same subject, the serum was in
some cases effective at slightly lower concentrations (higher titres).
Human complement did not affect neutralization titres. These findings
indicate that genetically diverse HIV-1 isolates carry both variable and
widely conserved antigenic epitopes for neutralizing antibodies. The
identification of shared epitopes may help the development of protective
vaccines.
Registry Numbers
0 (Antibodies, Viral). 0 (Antigens, Viral). 0 (Epitopes). 0 (HIV
Antibodies). 0 (HIV Antigens). 0 (Recombinant Proteins). 0 (Viral
Envelope Proteins). 9007-36-7 (Complement).
<9>
Unique Identifier
87184320
Authors
Tindall B. Cooper DA. Burcham J. Gold J. Penny R.
Title
Clinical and immunologic sequelae of AIDS retrovirus infection.
Source
Australian & New Zealand Journal of Medicine. 16(6):749-56, 1986 Dec.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/co [Complications]
*Acquired Immunodeficiency Syndrome/im [Immunology]
Antibodies, Viral/an [Analysis]
Australia
Homosexuality
Human
HIV/im [Immunology]
Male
Prospective Studies
Support, Non-U.S. Gov't
T-Lymphocytes/im [Immunology]
Abstract
The Sydney AIDS Project is a prospective immunoepidemiological study of
911 homosexual and bisexual men enrolled between February 1984 and January
1985. Clinical, immunological, and serological studies are performed on
these subjects every six months. At enrollment, 39.9% of subjects were
seropositive for antibodies to AIDS retrovirus (ARV). Of these 352
seropositive subjects, 28.1% were symptomless with normal immune profiles,
23.6% were symptomless with an immunodeficiency, 18.8% had a clinical
illness but normal immune profile, and 29.6% had a clinical illness and
immunodeficiency. Of the symptomless subjects, 27.8% were seropositive for
antibodies to ARV. Clinically, seropositivity was significantly associated
with enlargement of three or more non-inguinal lymph node groups,
splenomegaly, and hepatomegaly. Immunologically, seropositivity was
significantly associated with lower absolute numbers of lymphocytes and
T4+ lymphocytes and a lower T4+ : T8+ ratio, compared with seronegative
subjects. Seropositive subjects with a clinical illness had a
significantly lower percentage of T4+ lymphocytes and lower T4+ : T8+
ratio than did those who were symptomless. However, the absolute number of
T4+ cells was not significantly different between subjects with a clinical
illness and those who were symptomless. Subjects whose sera were positive
by immunofluorescence and enzyme-linked immunosorbent assay but were
negative by radioimmune precipitation assay had a lower number and
percentage of T4+ lymphocytes than subjects who were positive by all three
tests. These results demonstrate a wide variety of clinical and
immunological responses to ARV infection. Prospective study of these
subjects will enable us to define further the natural history of ARV
infection and factors associated with progression.
Registry Numbers
0 (Antibodies, Viral). 0 (HIV Antibodies).
<10>
Unique Identifier
87075776
Authors
Streilein JW. Parks WP.
Title
On the pathogenesis of immune incompetence in the acquired immune
deficiency syndrome.
Source
Bioessays. 4(6):286-91, 1986 Jun.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/et [Etiology]
*Acquired Immunodeficiency Syndrome/im [Immunology]
B-Lymphocytes/im [Immunology]
Human
HIV/im [Immunology]
T-Lymphocytes/im [Immunology]
<11>
Unique Identifier
87009907
Authors
Shearer GM. Bernstein DC. Tung KS. Via CS. Redfield R. Salahuddin SZ.
Gallo RC.
Title
A model for the selective loss of major histocompatibility complex
self-restricted T cell immune responses during the development of acquired
immune deficiency syndrome (AIDS).
Source
Journal of Immunology. 137(8):2514-21, 1986 Oct 15.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/im [Immunology]
Antibodies, Viral/an [Analysis]
AIDS-Related Complex/im [Immunology]
Human
HIV/im [Immunology]
HLA Antigens/an [Analysis]
Isoantigens/an [Analysis]
Lymphocyte Transformation
*Major Histocompatibility Complex
T-Lymphocytes/cl [Classification]
*T-Lymphocytes/im [Immunology]
T-Lymphocytes, Cytotoxic/im [Immunology]
Abstract
Functional analyses of peripheral blood leukocytes (PBL) from high risk
HTLV-III antibody-negative and antibody-positive donors, as well as from
patients with acquired immune deficiency syndrome (AIDS), lymphadenopathy
syndrome (LAS), and AIDS-related complex (ARC) were performed by the in
vitro generation of cytotoxic T lymphocyte (CTL) and proliferative
responses to the HLA self-restricted antigens of influenza virus (S + X)
and to nonself restricted HLA alloantigens (ALLO). All 40
antibody-negative donors tested responded to both S + X and ALLO in the
CTL response, whereas six of 14 antibody-positive, two of three LAS, four
of five ARC, and seven of 17 AIDS patients exhibited a selective absence
of CTL to S + X, but generated normal or elevated CTL responses to ALLO.
Of the remaining 10 AIDS patients, nine did not respond to either S + X or
ALLO, and one responded to both S + X and ALLO. A similar selective loss
of the proliferative response to S + X was found. We also observed
antibody-positive donors who initially generated CTL responses to S + X
and ALLO, but lost the S + X response as a function of time. We were able
to restore the selective loss of S + X CTL activity in vitro by the
addition of IL 2 and, to some extent, by co-stimulation with S + X plus
ALLO. Depletion of CD4+ T helper cells and removal of autologous
antigen-presenting cells from the PBL of healthy antibody-negative donors
indicated that distinct T helper cell subsets exist in human PBL, and that
S + X responses must use a CD4+ T helper population, whereas ALLO
responses can utilize an alternate CD4- T helper pathway. A model is
presented indicating the selective depletion of CD4+ T helper function in
the developmental stages of AIDS. The functional test for T helper
activity to self restricted antigens may be the earliest indicator of
immune functional loss in the development of AIDS, and may precede a
reduction in the absolute number of CD4+ cells.
Registry Numbers
0 (Antibodies, Viral). 0 (HIV Antibodies). 0 (HLA Antigens). 0
(Isoantigens).
<12>
Unique Identifier
87078258
Authors
Rial WY.
Title
Acquired immune deficiency syndrome.
Source
Clinical Therapeutics. 8(6):590-3, 1986.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/di [Diagnosis]
Acquired Immunodeficiency Syndrome/pc [Prevention & Control]
*Acquired Immunodeficiency Syndrome
Antibodies, Viral/an [Analysis]
Diagnosis, Differential
Ethics, Medical
Health Priorities
Human
HIV/im [Immunology]
United States
Registry Numbers
0 (Antibodies, Viral). 0 (HIV Antibodies).
<13>
Unique Identifier
87128385
Authors
Lepe-Zuniga JL. Mansell PW.
Title
AIDS: from immunity to infection to autoimmunity. A comprehensive
hypothesis of the pathogenesis of the disease.
Source
AIDS Research. 2(4):363-8, 1986 Fall.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/et [Etiology]
Acquired Immunodeficiency Syndrome/im [Immunology]
Autoantibodies/bi [Biosynthesis]
Human
HIV/py [Pathogenicity]
Immunity
Registry Numbers
0 (Autoantibodies).
<14>
Unique Identifier
87094337
Authors
Gras C. Renoux E.
Title
[AIDS]. [French]
Original Title
Le SIDA.
Source
Soins. (487-488):4-8, 1986 Oct.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/im [Immunology]
*Acquired Immunodeficiency Syndrome/pa [Pathology]
Acquired Immunodeficiency Syndrome/tm [Transmission]
Human
HIV/im [Immunology]
Opportunistic Infections/et [Etiology]
Sarcoma, Kaposi's/et [Etiology]
<15>
Unique Identifier
87079467
Authors
Galbraith NS. McEvoy M. Sibellas M.
Title
The acquired immune deficiency syndrome--1985.
Source
Community Medicine. 8(4):329-36, 1986 Nov.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/ep [Epidemiology]
Acquired Immunodeficiency Syndrome/pc [Prevention & Control]
Acquired Immunodeficiency Syndrome/tm [Transmission]
Female
Great Britain
Homosexuality
Human
HIV/im [Immunology]
Male
Pregnancy
<16>
Unique Identifier
87051399
Authors
Reitz MS. Gallo RC.
Title
Retroviruses of human T cells: their role in the aetiology of adult T-cell
leukaemia/lymphoma and the acquired immune deficiency syndrome.
Source
Cancer Surveys. 4(2):313-29, 1985.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/mi [Microbiology]
Genes, Viral
Human
HIV/ge [Genetics]
*HIV/py [Pathogenicity]
*HTLV-BLV Infections/mi [Microbiology]
HTLV-BLV Viruses/ge [Genetics]
*HTLV-BLV Viruses/py [Pathogenicity]
*Lymphoma/mi [Microbiology]
Transcription, Genetic
<17>
Unique Identifier
87030776
Authors
Goedert JJ. Gallo RC.
Title
Epidemiological evidence that HTLV-III is the AIDS agent.
Source
European Journal of Epidemiology. 1(3):155-9, 1985 Sep.
MeSH Subject Headings
Acquired Immunodeficiency Syndrome/ep [Epidemiology]
*Acquired Immunodeficiency Syndrome/mi [Microbiology]
Acquired Immunodeficiency Syndrome/tm [Transmission]
Antibodies, Viral/an [Analysis]
AIDS-Related Complex/ep [Epidemiology]
AIDS-Related Complex/mi [Microbiology]
AIDS-Related Complex/tm [Transmission]
Blood Transfusion/ae [Adverse Effects]
Female
Hemophilia/mi [Microbiology]
Hemophilia/th [Therapy]
Homosexuality
Human
HIV/ge [Genetics]
HIV/im [Immunology]
*HIV/ip [Isolation & Purification]
Male
Risk
T-Lymphocytes, Helper-Inducer/im [Immunology]
United States
Abstract
Human T-lymphotropic virus type III (HTLV-III) is a recently discovered
retrovirus with tropism and cytotoxicity for the OKT4+ lymphocytes that
are depleted in the acquired immune deficiency syndrome (AIDS). In
addition to the frequent detection of HTLV-III in patients with AIDS and
related syndromes, seroepidemiological studies have shown that HTLV-III
can be transmitted by sexual contact and blood transfusion in a manner
identical to the putative AIDS agent. Analyses of stored sera have
revealed that HTLV-III antibodies appeared in high-risk groups some two
years before the disease outbreak, which corresponds to the apparent
incubation period in patients with transfusion-associated AIDS. The risk
of developing AIDS is clearly associated with HTLV-III seropositivity and
may be as high as 20% within three years. Strong evidence that HTLV-III is
the AIDS agent mandates aggressive efforts to minimize further sexual,
maternal-fetal, and blood-borne transmission of this virus while pursuing
vaccine development and antiretroviral therapies.
Registry Numbers
0 (Antibodies, Viral). 0 (HIV Antibodies).
<18>
Unique Identifier
91026543
Authors
Gallo RC. Reitz MS Jr.
Institution
Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda,
Maryland 20205.
Title
The first human retroviruses: are there others?. [Review] [66 refs]
Source
Microbiological Sciences. 2(4):97-8, 101-4, 1985.
MeSH Subject Headings
*Acquired Immunodeficiency Syndrome/mi [Microbiology]
Human
*HIV
*HTLV-I
*HTLV-II
*Leukemia-Lymphoma, T-Cell, Acute, HTLV-I-Associated/mi [Microbiology]
Abstract
Three related, but very different, retroviruses have recently been
identified in man. Human T-cell leukaemia virus (HTLV) type I apparently
causes adult T-cell leukaemia. HTLV type II has been isolated only rarely
and has not been identified with a disease. HTLV type III is very likely
the causative agent in acquired immunodeficiency syndrome. [References:
66]