Pubmed

PMID- 21108852
OWN - NLM
STAT- MEDLINE
DA - 20101223
DCOM- 20110131
IS - 1743-422X (Electronic)
IS - 1743-422X (Linking)
VI - 7
DP - 2010
TI - Hepatitis C virus, human immunodeficiency virus and Pseudomonas phage PS5
triad
share epitopes of immunogenic determinants.
PG - 346
AB - A lytic phage for Pseudomonas aeruginosa belongs to the Myoviridea family
was
isolated from urine for use in therapeutics. Pair of hepatitis C virus (HC
V)
primers highlighted segments on the genome of this phage. The sequence of
these
PCR products as well as the possible serological cross reactivity/relation
ship
between HCV and the phage were investigated. One hundred HCV positive huma
n sera
were analyzed by ELISA. Ninety six well plates were coated with multiple e
pitopes
of HCV proteins (Kit), phage and Pseudomonas cells. Initially the positive
and
negative control sera supplied in the test kit were used to evaluate the c
ross
reactivity between the phage and anti-HCV antibodies. The results suggeste
d a
value over than 0.105 for a HCV positive reaction. Of the 100 HCV positive
sera
tested, sixty five and thirty percent showed cross reaction with phage lys
ate and
Pseudomonas aeruginosa, respectively. High HCV antibody titer correlated t
o high
cut off value for phage cross reaction, whereas no such correlation existe
d
between HCV antibody titer and Pseudomonas cross reaction. The PCR product
s were
sequenced and aligned with the HCV genome of H77. Sequence homology was de
tected
in the 5', 3' UTRs and NS3 regions. Further these products showed similari
ty with
HIV-1 Env, Pol & 3'LTR regions as well.
AD - No.102, Department of Microbiology, University of Karachi, Karachi, Pakist
an.
zhabizg@yahoo.com
FAU - Golkar, Zhabiz
AU - Golkar Z
FAU - Jamil, Nusrat
AU - Jamil N
LA - eng
PT - Journal Article
DEP - 20101126
PL - England
TA - Virol J
JT - Virology journal
JID - 101231645
RN - 0 (DNA, Viral)
RN - 0 (Epitopes)
RN - 0 (Hepatitis C Antibodies)
RN - 0 (RNA, Viral)
RN - 0 (Viral Proteins)
SB - IM
MH - *Cross Reactions
MH - DNA, Viral/genetics
MH - Epitopes/*immunology
MH - Female
MH - HIV-1/genetics/*immunology
MH - Hepacivirus/genetics/*immunology
MH - Hepatitis C Antibodies/*immunology
MH - Humans
MH - Pseudomonas Phages/genetics/*immunology
MH - Pseudomonas aeruginosa/immunology
MH - RNA, Viral/genetics
MH - Sequence Analysis, DNA
MH - Sequence Homology
MH - Viral Proteins/*immunology
MH - Young Adult
PMC - PMC3006387
OID - NLM: PMC3006387
EDAT- 2010/11/27 06:00
MHDA- 2011/02/01 06:00
CRDT- 2010/11/27 06:00
PHST- 2010/05/13 [received]
PHST- 2010/11/26 [accepted]
PHST- 2010/11/26 [aheadofprint]
AID - 1743-422X-7-346 [pii]
AID - 10.1186/1743-422X-7-346 [doi]
PST - epublish
SO - Virol J. 2010 Nov 26;7:346.
PMID- 21108831
OWN - NLM
STAT- MEDLINE
DA - 20101224
DCOM- 20110131
VI - 7
DP - 2010
TI - CD26/dipeptidyl peptidase IV (CD26/DPPIV) is highly expressed in periphera
l blood
of HIV-1 exposed uninfected female sex workers.
PG - 343
AB - BACKGROUND: Design of effective vaccines against the human immunodeficienc
y virus
(HIV-1) continues to present formidable challenges. However, individuals w
ho are
exposed HIV-1 but do not get infected may reveal correlates of protection
that
may inform on effective vaccine design. A preliminary gene expression anal
ysis of
HIV resistant female sex workers (HIV-R) suggested a high expression CD26/
DPPIV
gene. Previous studies have indicated an anti-HIV effect of high CD26/DPPI
V
expressing cells in vitro. Similarly, high CD26/DPPIV protein levels in vi
vo have
been shown to be a risk factor for type 2 diabetes. We carried out a study
to
confirm if the high CD26/DPPIV gene expression among the HIV-R were concor
dant
with high blood protein levels and its correlation with clinical type 2 di
abetes
and other perturbations in the insulin signaling pathway. RESULTS: A quant
itative
CD26/DPPIV plasma analysis from 100 HIV-R, 100 HIV infected (HIV +) and 10
0 HIV
negative controls (HIV Neg) showed a significantly elevated CD26/DPPIV
concentration among the HIV-R group (mean 1315 ng/ml) than the HIV Neg (91
0
ng/ml) and HIV + (870 ng/ml, p < 0.001). Similarly a FACs analysis of cell
associated DPPIV (CD26) revealed a higher CD26/DPPIV expression on CD4+ T-
cells
derived from HIV-R than from the HIV+ (90.30% vs 80.90 p = 0.002) and HIV
Neg
controls (90.30% vs 82.30 p < 0.001) respectively. A further comparison of
the
mean fluorescent intensity (MFI) of CD26/DPPIV expression showed a higher
DPP4
MFI on HIV-R CD4+ T cells (median 118 vs 91 for HIV-Neg, p = 0.0003). An
evaluation for hyperglycemia, did not confirm Type 2 diabetes but an impai
red
fasting glucose condition (5.775 mmol/L). A follow-up quantitative PCR ana
lysis
of the insulin signaling pathway genes showed a down expression of NFkappa
B, a
central mediator of the immune response and activator of HIV-1 transcripti
on.
CONCLUSION: HIV resistant sex workers have a high expression of CD26/DPPIV
in
tandem with lowered immune activation markers. This may suggest a novel ro
le for
CD26/DPPIV in protection against HIV infection in vivo.
AD - Centre For Virus Research, Mbagathi Road Kenya Medical Research Institute,
Nairobi, Kenya. Songok@cc.umanitoba.ca
FAU - Songok, Elijah M
AU - Songok EM
FAU - Osero, Bernard
AU - Osero B
FAU - McKinnon, Lyle
AU - McKinnon L
FAU - Rono, Martin K
AU - Rono MK
FAU - Apidi, Winnie
AU - Apidi W
FAU - Matey, Elizabeth J
AU - Matey EJ
FAU - Meyers, Adrienne F A
AU - Meyers AF
FAU - Luo, Ma
AU - Luo M
FAU - Kimani, Joshua
AU - Kimani J
FAU - Wachihi, Charles
AU - Wachihi C
FAU - Ball, Blake T
AU - Ball BT
FAU - Plummer, Frank A
AU - Plummer FA
FAU - Mpoke, Solomon
AU - Mpoke S
LA - eng
PT - Research Support, Non-U.S. Gov't
DEP - 20101125
PL - England
TA - Virol J
JID - 101231645
RN - 0 (NF-kappa B)
RN - EC 3.4.14.5 (DPP4 protein, human)
RN - EC 3.4.14.5 (Dipeptidyl Peptidase 4)
SB - IM
MH - CD4-Positive T-Lymphocytes/*chemistry
MH - Dipeptidyl Peptidase 4/analysis/*blood
MH - Female
MH - Gene Expression Profiling
MH - HIV/*immunology
MH - HIV-1/*immunology
MH - Humans
MH - *Immunity, Innate
MH - NF-kappa B/biosynthesis
MH - *Prostitution
PMC - PMC3009705
EDAT- 2010/11/27 06:00
MHDA- 2011/02/01 06:00
CRDT- 2010/11/27 06:00
AID - 1743-422X-7-343 [pii]
AID - 10.1186/1743-422X-7-343 [doi]
PST - epublish
SO - Virol J. 2010 Nov 25;7:343.
PMID- 21092135
OWN - NLM
STAT- MEDLINE
DA - 20101217
DCOM- 20110131
VI - 7
DP - 2010
TI - Human TOP1 residues implicated in species specificity of HIV-1 infection a
re
required for interaction with BTBD2, and RNAi of BTBD2 in old world monkey
and
human cells increases permissiveness to HIV-1 infection.
PG - 332
AB - BACKGROUND: Host determinants of HIV-1 viral tropism include factors from
producer cells that affect the efficiency of productive infection and fact
ors in
target cells that block infection after viral entry. TRIM5alpha restricts
HIV-1
infection at an early post-entry step through a mechanism associated with
rapid
disassembly of the retroviral capsid. Topoisomerase I (TOP1) appears to pl
ay a
role in HIV-1 viral tropism by incorporating into or otherwise modulating
virions
affecting the efficiency of a post-entry step, as the expression of human
TOP1 in
African Green Monkey (AGM) virion-producing cells increased the infectivit
y of
progeny virions by five-fold. This infectivity enhancement required human
TOP1
residues 236 and 237 as their replacement with the AGM counterpart residue
s
abolished the infectivity enhancement. Our previous studies showed that TO
P1
interacts with BTBD1 and BTBD2, two proteins which co-localize with the
TRIM5alpha splice variant TRIM5delta in cytoplasmic bodies. Because BTBD1
and
BTBD2 interact with one HIV-1 viral tropism factor, TOP1, and co-localize
with a
splice variant of another, we investigated the potential involvement of BT
BD1 and
BTBD2 in HIV-1 restriction. RESULTS: We show that the interaction of BTBD1
and
BTBD2 with TOP1 requires hu-TOP1 residues 236 and 237, the same residues r
equired
to enhance the infectivity of progeny virions when hu-TOP1 is expressed in
AGM
producer cells. Additionally, interference with the expression of BTBD2 in
AGM
and human 293T target cells increased their permissiveness to HIV-1 infect
ion
two- to three-fold. CONCLUSIONS: These results do not exclude the possibil
ity
that BTBD2 may modestly restrict HIV-1 infection via colocation with TRIM5
variants in cytoplasmic bodies.
AD - Department of Pathology, Uniformed Services University of the Health Scien
ces,
4301 Jones Bridge Road, Bethesda, MD 20814, USA.
FAU - Khurana, Bharat
AU - Khurana B
FAU - Zhuang, Lei
AU - Zhuang L
FAU - Moitra, Prasun K
AU - Moitra PK
FAU - Stantchev, Tzanko S
AU - Stantchev TS
FAU - Broder, Christopher C
AU - Broder CC
FAU - Cutler, Mary Lou
AU - Cutler ML
FAU - D'Arpa, Peter
AU - D'Arpa P
LA - eng
GR - R01CA059750/CA/NCI NIH HHS/United States
PT - Research Support, N.I.H., Extramural
DEP - 20101120
PL - England
TA - Virol J
JID - 101231645
RN - 0 (BTBD1 protein, human)
RN - 0 (BTBD2 protein, human)
RN - 0 (Carrier Proteins)
RN - 0 (DNA-Binding Proteins)
RN - 0 (Transcription Factors)
RN - EC 5.99.1.2 (DNA Topoisomerases, Type I)
RN - EC 5.99.1.2 (TOP1 protein, human)
SB - IM
MH - Animals
MH - Carrier Proteins/antagonists & inhibitors/*metabolism
MH - Cell Line
MH - Cercopithecus aethiops
MH - DNA Topoisomerases, Type I/*metabolism
MH - DNA-Binding Proteins/metabolism
MH - Gene Silencing
MH - HIV-1/*immunology/physiology
MH - *Host Specificity
MH - Humans
MH - Models, Molecular
MH - *Protein Interaction Mapping
MH - Transcription Factors/metabolism
PMC - PMC3002306
EDAT- 2010/11/26 06:00
MHDA- 2011/02/01 06:00
CRDT- 2010/11/25 06:00
AID - 1743-422X-7-332 [pii]
AID - 10.1186/1743-422X-7-332 [doi]
PST - epublish
SO - Virol J. 2010 Nov 20;7:332.
PMID- 21038473
OWN - NLM
STAT- MEDLINE
DA - 20101029
DCOM- 20101101
IS - 1537-6613 (Electronic)
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Proceedings of the International Symposium on Natural Immunity to HIV. Win
nipeg,
Manitoba, Canada. November 2009.
PG - S327-86
LA - eng
PT - Congresses
PT - Overall
PL - United States
TA - J Infect Dis
JT - The Journal of infectious diseases
JID - 0413675
SB - AIM
SB - IM
MH - HIV Infections/*immunology
MH - Humans
MH - Immunity, Innate
EDAT- 2010/11/03 06:00
MHDA- 2010/11/03 06:01
CRDT- 2010/11/02 06:00
PST - ppublish
SO - J Infect Dis. 2010 Nov 1;202 Suppl 3:S327-86.
PMID- 21034678
OWN - NLM
STAT- MEDLINE
DA - 20101101
DCOM- 20110202
IS - 1539-6509 (Linking)
VI - 10
IP - 53
DP - 2010 Oct
TI - Some unmet challenges in the immunology of viral infections.
PG - 363-70
AB - Viral immunology is a rapidly evolving field. Major strides have been made
in our
understanding of innate and adaptive immune responses to viruses, largely
based
on highly reductionistic animal infection models, but more recently in hum
ans,
with validation that fundamental immunological concepts do in fact transla
te into
clinical science well. From these studies there has emerged an appreciatio
n of
the enormous complexity of the immune response to viral infections as well
as the
diverse array of strategies developed by viruses to deal with immune detec
tion.
In this review, we highlight some of the major challenges we face in unrav
eling
this complexity and summarize current efforts under way to improve the eff
icacy
of viral vaccines.
AD - Department of Pathobiology, College of Veterinary Medicine, University of
Tennessee, Knoxville, Tennessee 37996, USA. btr@utk.edu
FAU - Rouse, Barry T
AU - Rouse BT
FAU - Lukacher, Aron E
AU - Lukacher AE
LA - eng
GR - R01 AI106336501/AI/NIAID NIH HHS/United States
GR - R01 CA139220/CA/NCI NIH HHS/United States
GR - R01 CA71971/CA/NCI NIH HHS/United States
GR - R01 EY05093/EY/NEI NIH HHS/United States
PT - Review
PL - United States
TA - Discov Med
JT - Discovery medicine
JID - 101250006
RN - 0 (Viral Vaccines)
SB - IM
MH - HIV/immunology
MH - Hepacivirus/immunology
MH - Humans
MH - Immunity, Innate/physiology
MH - Influenza A Virus, H1N1 Subtype/immunology
MH - Treatment Outcome
MH - Vaccination/methods
MH - Viral Vaccines/immunology/therapeutic use
MH - Virus Diseases/*immunology/*therapy
MH - Viruses/*immunology
EDAT- 2010/11/03 06:00
MHDA- 2011/02/03 06:00
CRDT- 2010/11/02 06:00
PST - ppublish
SO - Discov Med. 2010 Oct;10(53):363-70.
PMID- 20977343
OWN - NLM
STAT- MEDLINE
DA - 20101104
DCOM- 20101210
IS - 0022-1899 (Linking)
VI - 202
IP - 11
DP - 2010 Dec 1
TI - IL28B polymorphism does not determine outcomes of hepatitis B virus or HIV
infection.
PG - 1749-53
AB - An IL28B haplotype strongly determines the outcome of natural and
interferon-alpha treated hepatitis C virus (HCV) infection. To assess whet
her the
polymorphism marking the haplotype (rs12979860) also affects other
interferon-alpha responsive chronic viral illnesses, namely hepatitis B vi
rus
(HBV) and human immunodeficiency virus (HIV) type 1 infections, we genotyp
ed 226
individuals with HBV persistence, 384 with HBV recovery, and 2548 with or
at high
risk for HIV infection. The C/C genotype of rs12979860 was not associated
with
HBV recovery (odds ratio, 0.99), resistance to HIV infection (odds ratio,
0.97),
or HIV disease progression (P > .05). This IL28B single-nucleotide polymor
phism
affects the immune response to HCV but not to HBV or HIV.
AD - Cancer and Inflammation Program, Laboratory of Experimental Immunology,
SAIC-Frederick, NCI-Frederick, Frederick, Maryland, USA.
FAU - Martin, Maureen P
AU - Martin MP
FAU - Qi, Ying
AU - Qi Y
FAU - Goedert, James J
AU - Goedert JJ
FAU - Hussain, Shehnaz K
AU - Hussain SK
FAU - Kirk, Gregory D
AU - Kirk GD
FAU - Hoots, W Keith
AU - Hoots WK
FAU - Buchbinder, Susan
AU - Buchbinder S
FAU - Carrington, Mary
AU - Carrington M
FAU - Thio, Chloe L
AU - Thio CL
LA - eng
GR - 5-MO1-RR-00722/RR/NCRR NIH HHS/United States
GR - MO1-RR00059/RR/NCRR NIH HHS/United States
GR - N01-CO-12400/CO/NCI NIH HHS/United States
GR - N01-HD-4-3200/HD/NICHD NIH HHS/United States
GR - N02-CP-55504/CP/NCI NIH HHS/United States
GR - R01-DA-04334/DA/NIDA NIH HHS/United States
GR - R01-DA-12568/DA/NIDA NIH HHS/United States
GR - R01-HD-4-1224/HD/NICHD NIH HHS/United States
GR - UO1-AI-35039/AI/NIAID NIH HHS/United States
PT - Research Support, N.I.H., Intramural
PT - Research Support, U.S. Gov't, P.H.S.
DEP - 20101026
PL - United States
TA - J Infect Dis
JID - 0413675
RN - 0 (IL28B protein, human)
RN - 0 (Interleukins)
SB - AIM
SB - IM
MH - Adult
MH - Case-Control Studies
MH - Cohort Studies
MH - Female
MH - Genotype
MH - Hepacivirus
MH - Hepatitis B/*immunology
MH - Hepatitis B virus/*immunology
MH - Hepatitis C
MH - Humans
MH - Interleukins/*genetics/immunology
MH - Male
MH - *Polymorphism, Single Nucleotide
MH - Proportional Hazards Models
MH - Young Adult
PMC - PMC2974014
MID - NIHMS233857
OID - NLM: NIHMS233857 [Available on 12/01/11]
OID - NLM: PMC2974014 [Available on 12/01/11]
EDAT- 2010/10/28 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/10/28 06:00
PMCR- 2011/12/01
AID - 10.1086/657146 [doi]
PST - ppublish
SO - J Infect Dis. 2010 Dec 1;202(11):1749-53. Epub 2010 Oct 26.
PMID- 20972328
OWN - NLM
STAT- MEDLINE
DA - 20101102
DCOM- 20101207
LR - 20110103
IS - 0021-9738 (Linking)
VI - 120
IP - 11
DP - 2010 Nov 1
TI - New therapy to revert dysfunctional antibody responses during HIV-1 infect
ion.
PG - 3810-3
LID - 10.1172/JCI44872 [doi]
LID - 44872 [pii]
AB - Individuals infected with HIV-1 progress to AIDS at different rates. Rapid
progressors develop AIDS within 2-5 years of initial infection, compared w
ith
approximately 10 years in typical progressors. Progression to AIDS is asso
ciated
with impaired humoral and cellular immunity. In this issue of the JCI, Tit
anji
and colleagues report that activated memory B (mBAct) cells are depleted i
n
SIV-infected macaques defined as rapid progressors. Depletion was mediated
by
programmed death-1 (PD-1) and resulted in reduction of antibody titers spe
cific
for SIV and bacterial antigens. Interestingly, blockade of PD-1 in infecte
d
animals protected B cells from apoptosis and increased levels of SIV-speci
fic
antibodies in blood. These findings pave the way for a new therapeutic str
ategy
aimed at improving humoral immunity in HIV-1 infection.
AD - Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet,
Stockholm, Sweden. francesca.chiodi@ki.se
FAU - Chiodi, Francesca
AU - Chiodi F
LA - eng
PT - Comment
DEP - 20101025
PL - United States
TA - J Clin Invest
JT - The Journal of clinical investigation
JID - 7802877
RN - 0 (Antibodies, Viral)
RN - 0 (Antigens, CD)
SB - AIM
SB - IM
CON - J Clin Invest. 2010 Nov 1;120(11):3878-90. PMID: 20972331
MH - Animals
MH - Antibodies, Viral/blood/immunology
MH - *Antibody Formation
MH - Antigens, CD/immunology
MH - CD8-Positive T-Lymphocytes/immunology
MH - Cell Differentiation
MH - Cell Survival
MH - *HIV Infections/drug therapy/immunology/physiopathology
MH - Humans
MH - Immunologic Memory/*immunology
MH - Lymphoid Tissue/cytology/immunology
MH - *Simian Acquired Immunodeficiency Syndrome/drug
therapy/immunology/physiopathology
MH - Simian immunodeficiency virus/*immunology
PMC - PMC2965000
EDAT- 2010/10/26 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/10/26 06:00
AID - 44872 [pii]
AID - 10.1172/JCI44872 [doi]
PST - ppublish
SO - J Clin Invest. 2010 Nov 1;120(11):3810-3. doi: 10.1172/JCI44872. Epub 2010
Oct
25.
PMID- 20966557
OWN - NLM
STAT- MEDLINE
DA - 20101022
DCOM- 20110214
IS - 0255-0857 (Linking)
VI - 28
IP - 4
DP - 2010 Oct-Dec
TI - Evaluation of Calypte AWARE HIV-1/2 OMT antibody test as a screening test
in an
Indian setting.
PG - 295-8
AB - PURPOSE: Integrated counselling and testing centres (ICTC) provide counsel
ling
and blood testing facilities for HIV diagnosis. Oral fluid tests provide a
n
alternative for people who do not want blood to be drawn. Also, it avoids
the
risk of occupational exposure. The goal of this study was to evaluate the
utility
of Calypte AWARE HIV-1/2 OMT antibody test as a screening test in an India
n
setting. MATERIALS AND METHODS: A cross-sectional study was carried out af
ter
ethics committee approval in 250 adult ICTC clients. Blood was collected a
nd
tested from these clients for HIV diagnosis as per routine policy and the
results
were considered as the gold standard. Also, after another written informed
consent, oral fluid was collected from the clients and tested for the pres
ence of
HIV antibodies. Twenty five clients who had and 25 clients who had not com
pleted
their secondary school education (Group A and Group B, respectively) were
also
asked to perform and interpret the test on their own and their findings an
d
experiences were noted. RESULT: The sensitivity, specificity, PPV and NPV
of the
oral fluid antibody test were 100%, 98.51%, 94.11% and 100%, respectively.
Seventy six percent of clients preferred oral fluid testing. Group B found
it
difficult to perform the test as compared to Group A and this difference w
as
statistically significant (P </= 0.05). CONCLUSION: Oral fluid testing can
be
used as a screening test for HIV diagnosis; however, confirmation of react
ive
results by blood-based tests is a must.
AD - Department of Microbiology, Seth GSMC & KEMH, Parel, Mumbai, India.
nayanaingole@gmail.com
FAU - Ingole, N A
AU - Ingole NA
FAU - Mehta, P R
AU - Mehta PR
FAU - Bande, R N
AU - Bande RN
FAU - Paranjpe, S M
AU - Paranjpe SM
FAU - Wanjare, S W
AU - Wanjare SW
LA - eng
PT - Evaluation Studies
PL - India
TA - Indian J Med Microbiol
JT - Indian journal of medical microbiology
JID - 8700903
RN - 0 (HIV Antibodies)
RN - 0 (Reagent Kits, Diagnostic)
SB - IM
MH - AIDS Serodiagnosis/methods
MH - Adult
MH - Cross-Sectional Studies
MH - HIV Antibodies/analysis/*blood
MH - HIV Infections/*diagnosis/immunology/prevention & control/virology
MH - Humans
MH - India
MH - Male
MH - Mass Screening/*methods
MH - Predictive Value of Tests
MH - Reagent Kits, Diagnostic
MH - Saliva/*immunology
MH - Sensitivity and Specificity
EDAT- 2010/10/23 06:00
MHDA- 2011/02/15 06:00
CRDT- 2010/10/23 06:00
AID - IndianJMedMicrobiol_2010_28_4_295_71809 [pii]
AID - 10.4103/0255-0857.71809 [doi]
PST - ppublish
SO - Indian J Med Microbiol. 2010 Oct-Dec;28(4):295-8.
PMID- 20966556
OWN - NLM
STAT- MEDLINE
DA - 20101022
DCOM- 20110214
IS - 0255-0857 (Linking)
VI - 28
IP - 4
DP - 2010 Oct-Dec
TI - Study of HIV-1 subtypes in serodiscordant couples attending an integrated
counselling and testing centre in Mumbai using heteroduplex mobility analy
sis and
DNA sequencing.
PG - 290-4
AB - AIMS: To determine the prevalent subtypes of HIV-1 in serodiscordant coupl
es.
Setting: Integrated Counselling and Testing Centre (ICTC), Department of
Microbiology. STUDY DESIGN: Prospective pilot study. Participants: Thirty
HIV-1
serodiscordant couples. INCLUSION CRITERIA: a) Documentation of HIV-1 infe
ction
in one partner and seronegative status in the other, current history of co
ntinued
unprotected sexual activity within the partnership, demonstration that the
y have
been in a partnership for at least 1 year and are not currently on highly
active
antiretroviral therapy HAART; b) willingness of both partners to provide w
ritten
informed consent including consent to continued couple counselling for 3 m
onths.
MATERIALS AND METHODS: HIV-1 subtyping was carried out by heteroduplex mob
ility
analysis (HMA) by amplifying env region; and DNA sequencing by amplifying
gag
region. RESULTS: HIV-1 env gene was amplified successfully in 10/30 sample
s; gag
gene, in 25/30 samples; and both env and gag gene were amplified successfu
lly in
5/30 samples. HIV-1 subtype C was detected from 21 samples; subtype B, fro
m 7;
and subtype A, from 2. Sample from 1 positive partner was detected as subt
ype C
by env HMA and subtype B by gag sequencing. CONCLUSION: HIV-1 subtype C wa
s found
to be the predominant subtype of HIV-1 in serodiscordant couples attending
our
ICTC, followed by HIV-1 subtype B and HIV-1 subtype A, respectively. DNA
sequencing was found to be the most reliable method for determining the su
btypes
of HIV-1.
AD - Department of Microbiology, Seth GSMC & KEM Hospital, Mumbai, India.
prm.kem@gmail.com
FAU - Mehta, P R
AU - Mehta PR
FAU - Nema, S
AU - Nema S
FAU - Paranjpe, S
AU - Paranjpe S
FAU - Ingole, N
AU - Ingole N
FAU - Wanjare, S
AU - Wanjare S
FAU - Nataraj, G
AU - Nataraj G
LA - eng
PT - Evaluation Studies
PL - India
TA - Indian J Med Microbiol
JT - Indian journal of medical microbiology
JID - 8700903
RN - 0 (DNA, Viral)
SB - IM
MH - AIDS Serodiagnosis
MH - Counseling
MH - DNA, Viral/analysis/genetics
MH - Delivery of Health Care, Integrated
MH - *Family Characteristics
MH - Female
MH - Genes, env
MH - Genes, gag
MH - HIV Infections/epidemiology/*virology
MH - *HIV Seronegativity
MH - HIV-1/*classification/*genetics/immunology
MH - Heteroduplex Analysis/*methods
MH - Humans
MH - India/epidemiology
MH - Male
MH - Outpatient Clinics, Hospital
MH - Prevalence
MH - Sequence Analysis, DNA/*methods
EDAT- 2010/10/23 06:00
MHDA- 2011/02/15 06:00
CRDT- 2010/10/23 06:00
AID - IndianJMedMicrobiol_2010_28_4_290_71807 [pii]
AID - 10.4103/0255-0857.71807 [doi]
PST - ppublish
SO - Indian J Med Microbiol. 2010 Oct-Dec;28(4):290-4.
PMID- 20946627
OWN - NLM
STAT- MEDLINE
DA - 20101102
DCOM- 20101201
VI - 7
DP - 2010
TI - Anti-HIV-1 activity of salivary MUC5B and MUC7 mucins from HIV patients wi
th
different CD4 counts.
PG - 269
AB - BACKGROUND: We have previously shown that MUC5B and MUC7 mucins from saliv
a of
HIV negative individuals inhibit HIV-1 activity by 100% in an in vitro ass
ay. The
purpose of this subsequent study was to investigate whether MUC5B and MUC7
from
saliva of HIV patients or with full blown AIDS had a similar inhibitory ac
tivity
against the virus. METHODS: Salivary MUC5B and MUC7 from HIV patients with
different CD4 counts (< 200, 200-400 and > 400) were incubated with HIV-1
prior
to infection of the human T lymphoblastoid cell line (CEM SS cells). Cells
were
then cultured and viral replication was measured by a qualitative p24 anti
gen
assay. The size, charge and immunoreactivity of mucins from HIV negative a
nd
positive individuals was also analysed by SDS-PAGE, Western blot and ELISA
respectively. RESULTS: It was shown that irrespective of their CD4 counts
both
MUC5B and MUC7 from HIV patients, unlike the MUC5B and MUC7 from HIV negat
ive
individuals, did not inhibit HIV-1 activity. Size, charge and immunoreacti
vity
differences between the mucins from HIV negative and positive individuals
and
among the mucins from HIV patients of different CD4 count was observed by
SDS-PAGE, Western blot and ELISA. CONCLUSIONS: Purified salivary mucins fr
om HIV
positive patients do not inhibit the AIDS virus in an in vitro assay. Alth
ough
the reason for the inability of mucins from infected individuals to inhibi
t the
virus is not known, it is likely that there is an alteration of the glycos
ylation
pattern, and therefore of charge of mucin, in HIV positive patients. The a
bility
to inhibit the virus by aggregation by sugar chains is thus diminished.
AD - Department of Surgery, Division of General Surgery, University of Cape Tow
n,
Observatory, Cape 7925, South Africa.
FAU - Habte, Habtom H
AU - Habte HH
FAU - de Beer, Corena
AU - de Beer C
FAU - Lotz, Zoe E
AU - Lotz ZE
FAU - Roux, Paul
AU - Roux P
FAU - Mall, Anwar S
AU - Mall AS
LA - eng
DEP - 20101014
PL - England
TA - Virol J
JID - 101231645
RN - 0 (HIV Core Protein p24)
RN - 0 (MUC5B protein, human)
RN - 0 (MUC7 protein, human)
RN - 0 (Mucin-5B)
RN - 0 (Mucins)
RN - 0 (Salivary Proteins and Peptides)
SB - IM
MH - Blotting, Western
MH - CD4 Lymphocyte Count
MH - Cell Line
MH - Electrophoresis, Polyacrylamide Gel
MH - Enzyme-Linked Immunosorbent Assay
MH - Female
MH - HIV Core Protein p24/analysis
MH - HIV-1/*growth & development/*immunology
MH - Humans
MH - Molecular Weight
MH - Mucin-5B/chemistry/*immunology/isolation & purification
MH - Mucins/chemistry/*immunology/isolation & purification
MH - Salivary Proteins and Peptides/chemistry/*immunology/isolation & purificat
ion
PMC - PMC2967540
EDAT- 2010/10/16 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/10/16 06:00
AID - 1743-422X-7-269 [pii]
AID - 10.1186/1743-422X-7-269 [doi]
PST - epublish
SO - Virol J. 2010 Oct 14;7:269.
PMID- 20941398
OWN - NLM
STAT- MEDLINE
DA - 20101013
DCOM- 20110214
IS - 1553-7366 (Linking)
VI - 6
IP - 9
DP - 2010
TI - Phylogenetic approach reveals that virus genotype largely determines HIV
set-point viral load.
LID - e1001123 [pii]
AB - HIV virulence, i.e. the time of progression to AIDS, varies greatly among
patients. As for other rapidly evolving pathogens of humans, it is difficu
lt to
know if this variance is controlled by the genotype of the host or that of
the
virus because the transmission chain is usually unknown. We apply the
phylogenetic comparative approach (PCA) to estimate the heritability of a
trait
from one infection to the next, which indicates the control of the virus g
enotype
over this trait. The idea is to use viral RNA sequences obtained from pati
ents
infected by HIV-1 subtype B to build a phylogeny, which approximately refl
ects
the transmission chain. Heritability is measured statistically as the prop
ensity
for patients close in the phylogeny to exhibit similar infection trait val
ues.
The approach reveals that up to half of the variance in set-point viral lo
ad, a
trait associated with virulence, can be heritable. Our estimate is signifi
cant
and robust to noise in the phylogeny. We also check for the consistency of
our
approach by showing that a trait related to drug resistance is almost enti
rely
heritable. Finally, we show the importance of taking into account the
transmission chain when estimating correlations between infection traits.
The
fact that HIV virulence is, at least partially, heritable from one infecti
on to
the next has clinical and epidemiological implications. The difference bet
ween
earlier studies and ours comes from the quality of our dataset and from th
e power
of the PCA, which can be applied to large datasets and accounts for within
-host
evolution. The PCA opens new perspectives for approaches linking clinical
data
and evolutionary biology because it can be extended to study other traits
or
other infectious diseases.
AD - Institute of Integrative Biology, ETH Zurich, Zurich, Switzerland.
samuel.alizon@montp.cnrs.fr
FAU - Alizon, Samuel
AU - Alizon S
FAU - von Wyl, Viktor
AU - von Wyl V
FAU - Stadler, Tanja
AU - Stadler T
FAU - Kouyos, Roger D
AU - Kouyos RD
FAU - Yerly, Sabine
AU - Yerly S
FAU - Hirschel, Bernard
AU - Hirschel B
FAU - Boni, Jurg
AU - Boni J
FAU - Shah, Cyril
AU - Shah C
FAU - Klimkait, Thomas
AU - Klimkait T
FAU - Furrer, Hansjakob
AU - Furrer H
FAU - Rauch, Andri
AU - Rauch A
FAU - Vernazza, Pietro L
AU - Vernazza PL
FAU - Bernasconi, Enos
AU - Bernasconi E
FAU - Battegay, Manuel
AU - Battegay M
FAU - Burgisser, Philippe
AU - Burgisser P
FAU - Telenti, Amalio
AU - Telenti A
FAU - Gunthard, Huldrych F
AU - Gunthard HF
FAU - Bonhoeffer, Sebastian
AU - Bonhoeffer S
CN - Swiss HIV Cohort Study
LA - eng
DEP - 20100930
PL - United States
TA - PLoS Pathog
JT - PLoS pathogens
JID - 101238921
RN - 0 (Anti-HIV Agents)
RN - 0 (RNA, Viral)
SB - IM
MH - Anti-HIV Agents/therapeutic use
MH - Genotype
MH - HIV Infections/drug therapy/*genetics/*transmission
MH - HIV-1/*classification/*genetics
MH - Humans
MH - Models, Statistical
MH - *Phylogeny
MH - Quantitative Trait Loci
MH - RNA, Viral/genetics
MH - Viral Load/*genetics/*statistics & numerical data
PMC - PMC2947993
EDAT- 2010/10/14 06:00
MHDA- 2011/02/15 06:00
CRDT- 2010/10/14 06:00
PHST- 2010/09/30 [epublish]
AID - 10.1371/journal.ppat.1001123 [doi]
PST - epublish
SO - PLoS Pathog. 2010 Sep 30;6(9). pii: e1001123.
PMID- 20887229
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Genomic approaches to the study of HIV-1 acquisition.
PG - S382-6
AB - Host genome studies are increasingly available for the study of infectious
disease susceptibility. Current technologies include large-scale genotypin
g,
genome-wide screens such as transcriptome and silencing (silencing RNA) st
udies,
and increasingly, the possibility to sequence complete genomes. These appr
oaches
are of interest for the study of individuals who remain uninfected despite
documented exposure to human immunodeficiency virus type 1. The main limit
ation
remains the ascertainment of exposure and establishing large cohorts of
informative individuals. The pattern of enrichment for CCR5 Delta32 homozy
gosis
should serve as the standard for assessing the extent to which a given coh
ort (of
white subjects) includes a large proportion of exposed uninfected individu
als.
AD - Institute of Microbiology, University Hospital Center, University of Lausa
nne,
Lausanne, Switzerland. amalio.telenti@chuv.ch
FAU - Telenti, Amalio
AU - Telenti A
FAU - McLaren, Paul
AU - McLaren P
LA - eng
PT - Review
PL - United States
TA - J Infect Dis
JID - 0413675
SB - AIM
SB - IM
MH - Gene Expression Profiling
MH - Gene Silencing
MH - *Genetic Predisposition to Disease
MH - Genetic Testing/methods
MH - HIV Infections/*genetics/virology
MH - Humans
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655969 [doi]
PST - ppublish
PMID- 20887228
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Cohorts for the study of HIV-1-exposed but uninfected individuals: benefit
s and
limitations.
PG - S377-81
AB - Since the late 1980s, with the first identification of individuals who wer
e
exposed to human immunodeficiency virus type 1 (HIV-1) yet remained uninfe
cted,
or "HIV-1-resistant" individuals, a large number of cohorts that include
HIV-exposed seronegative (HESN) subjects have been identified globally for
the
purpose of investigating the genetic, immunologic, and environmental facto
rs that
may help alter susceptibility to HIV-1. In this article, in light of the r
ecent
International Symposium on Natural Immunity to HIV, we review the characte
ristics
of different groups with respect to their relative risks and briefly summa
rize
the known cohorts that include exposed uninfected subjects worldwide.
AD - Department of Medical Microbiology, University of Manitoba, Winnipeg, Mani
toba,
Canada.
FAU - Horton, R E
AU - Horton RE
FAU - McLaren, P J
AU - McLaren PJ
FAU - Fowke, K
AU - Fowke K
FAU - Kimani, J
AU - Kimani J
FAU - Ball, T Blake
AU - Ball TB
LA - eng
PT - Review
PL - United States
TA - J Infect Dis
JID - 0413675
SB - AIM
SB - IM
MH - Cohort Studies
MH - Disease Susceptibility
MH - Female
MH - HIV Infections/*immunology/*transmission
MH - Humans
MH - Male
MH - Risk Factors
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655971 [doi]
PST - ppublish
PMID- 20887225
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Innate immunity in resistance to HIV infection.
PG - S361-5
AB - Resistance to human immunodeficiency virus (HIV) infection in subjects who
do not
seroconvert despite multiple exposures to the virus and to the progression
to
AIDS in HIV‐infected individuals depends on multiple factors involv
ing
both the innate and the adaptive immune system. The contribution of natura
l
immunity in preventing HIV infection has so far received little attention,
but
many recently published articles suggest a key role for Toll‐like
receptors, natural killer cells, interleukin‐22, acute‐phase
amyloid A protein, and APOBEC3G in conferring resistance to HIV infection.
The
study of these factors will shed light on HIV pathogenesis and contribute
to the
development of new therapeutic approaches to this elusive disease.
AD - Department of Clinical Sciences, University of Milano, Milan, Italy.
mara.biasin@unimi.it
FAU - Biasin, Mara
AU - Biasin M
FAU - Clerici, Mario
AU - Clerici M
FAU - Piacentini, Luca
AU - Piacentini L
LA - eng
PL - United States
TA - J Infect Dis
JID - 0413675
RN - 0 (Interleukins)
RN - 0 (Serum Amyloid A Protein)
RN - 0 (Toll-Like Receptors)
RN - 0 (interleukin-22)
RN - EC 3.5.4.5 (APOBEC3G protein, human)
RN - EC 3.5.4.5 (Cytidine Deaminase)
SB - AIM
SB - IM
MH - Cytidine Deaminase/immunology
MH - Humans
MH - Interleukins/immunology
MH - Killer Cells, Natural/immunology
MH - Serum Amyloid A Protein/immunology
MH - Toll-Like Receptors/immunology
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655965 [doi]
PST - ppublish
PMID- 20887224
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Mind the gap: lack of association between KIR3DL1*004/HLA-Bw4-induced natu
ral
killer cell function and protection from HIV infection.
PG - S356-60
AB - Several combinations of genes encoding KIR3DL1 alleles and their HLA-Bw4 l
igands
have been linked with favorable outcomes upon exposure to or infection wit
h human
immunodeficiency virus (HIV). Some protective KIR3DL1/HLA-Bw4 combinations
confer
elevated natural killer (NK) cell functional potential. The K562-stimulate
d
functionality of NK cells from KIR3DL1*004/HLA-Bw4 and control genotype ca
rriers
was assessed by flow cytometry and found to be higher in KIR3DL1*004/HLA-B
w4
carriers. However, a comparison of the frequency of this combined genotype
among
HIV-exposed uninfected and HIV-infected subjects revealed no between-group
differences. Thus, despite its ability to license NK cells, KIR3DL1*004/HL
A-Bw4
is not associated with a reduced risk of infection.
AD - Research Institute of the McGill University Health Centre, Montreal, Quebe
c,
Canada.
FAU - Parsons, Matthew S
AU - Parsons MS
FAU - Boulet, Salix
AU - Boulet S
FAU - Song, Rujun
AU - Song R
FAU - Bruneau, Julie
AU - Bruneau J
FAU - Shoukry, Naglaa H
AU - Shoukry NH
FAU - Routy, Jean-Pierre
AU - Routy JP
FAU - Tsoukas, Christos M
AU - Tsoukas CM
FAU - Bernard, Nicole F
AU - Bernard NF
LA - eng
GR - HVI 79515/Canadian Institutes of Health Research/Canada
PL - United States
TA - J Infect Dis
JID - 0413675
RN - 0 (HLA-B Antigens)
RN - 0 (HLA-Bw4)
RN - 0 (KIR3DL1 protein, human)
RN - 0 (Receptors, KIR3DL1)
SB - AIM
SB - IM
MH - Gene Frequency
MH - HIV Infections/*genetics/*immunology
MH - HLA-B Antigens/*genetics
MH - Humans
MH - Killer Cells, Natural/*immunology
MH - Receptors, KIR3DL1/*genetics
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655966 [doi]
PST - ppublish
PMID- 20887223
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Innate molecular and anatomic mucosal barriers against HIV infection in th
e
genital tract of HIV-exposed seronegative individuals.
PG - S351-5
AB - Sexual transmission is the single most common mechanism for acquiring infe
ction
with human immunodeficiency virus (HIV), and the efficiency of transmissio
n
reflects the biology of the mucosal site. The localization and phenotypic
characterization of HIV target cells and receptors and the presence of imm
une
molecules are therefore important to define at sites of HIV exposure. To
complicate the picture, HIV‐binding receptors and antiviral immune
molecules can be protective under certain circumstances but can exert an o
pposite
effect at other mucosal sites, concentrations, and time points. Considerin
g the
additional physiological changes induced by inflammation, hormones, and se
men
deposition, it is an enormous challenge to design relevant experimental mo
dels
for evaluating prophylactic compounds or biological events. Studies in muc
osal
samples of HIV‐exposed seronegative individuals are among the many
opportunities to explore the biological events of HIV transmission under
physiological circumstances.
AD - Department of Medicine, Solna, Infectious Disease Unit, Center for Molecul
ar
Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm
,
Sweden. Kristina.broliden@karolinska.se
FAU - Broliden, Kristina
AU - Broliden K
LA - eng
PL - United States
TA - J Infect Dis
JID - 0413675
SB - AIM
SB - IM
MH - Female
MH - Genitalia/*anatomy & histology/*immunology
MH - HIV Infections/*immunology/transmission
MH - Humans
MH - Male
MH - Mucous Membrane/*anatomy & histology/*immunology
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655964 [doi]
PST - ppublish
PMID- 20887222
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Natural resistance to HIV infection: lessons learned from HIV-exposed unin
fected
individuals.
PG - S345-50
AB - We explored potential mechanisms of resistance to human immunodeficiency v
irus
type 1 (HIV-1) infection in different groups of uninfected individuals exp
osed by
systemic or mucosal routes: intravascular drug users in Vietnam and spouse
s of
HIV-infected individuals in Cambodia and Central African Republic. Our mai
n
findings were reduced susceptibility of peripheral blood mononuclear cells
to
HIV-1 infection in vitro, associated with low levels of CD4+ T cell activa
tion in
vivo and/or cell restriction of viral replication, and enhanced natural ki
ller
cell activity, associated with increased ratios of activating to inhibitor
y
natural killer cell receptors. These results support a contribution of inn
ate
responses to resistance against HIV-1 infection. Scientific and ethical is
sues
encountered during research in exposed uninfected subjects must be conside
red.
AD - Institut Pasteur, Unite de Regulation des Infections Retrovirales, Paris,
France.
gianfranco.pancino@pasteur.fr
FAU - Pancino, Gianfranco
AU - Pancino G
FAU - Saez-Cirion, Asier
AU - Saez-Cirion A
FAU - Scott-Algara, Daniel
AU - Scott-Algara D
FAU - Paul, Pascale
AU - Paul P
LA - eng
PL - United States
TA - J Infect Dis
JID - 0413675
SB - AIM
SB - IM
MH - Cambodia
MH - Central African Republic
MH - Female
MH - Humans
MH - Killer Cells, Natural/immunology
MH - Leukocytes, Mononuclear/*immunology/*virology
MH - Lymphocyte Activation
MH - Male
MH - Vietnam
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655973 [doi]
PST - ppublish
PMID- 20887221
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - HIV-exposed seronegative commercial sex workers show a quiescent phenotype
in the
CD4+ T cell compartment and reduced expression of HIV-dependent host facto
rs.
PG - S339-44
AB - Studies of human immunodeficiency virus (HIV)-exposed seronegative individ
uals
are crucial to inform vaccine design. In the present study we demonstrated
that
HIV-exposed seronegative commercial sex workers produce lower levels of
proinflammatory cytokines at baseline than HIV-negative control subjects.
We also
showed that CD4+ T cells of HIV-exposed seronegative commercial sex worker
s have
a characteristically lower level of gene expression that can be seen in
differentially expressed genes and systems crucial for HIV replication, su
ch as
the T cell receptor pathway and previously identified HIV dependency facto
rs.
This apparent lowered activation results in a phenomenon we term "immune
quiescence," which may contribute to host resistance to HIV.
AD - Department of Medical Microbiology, University of Manitoba, Ontario, Canad
a.
FAU - McLaren, Paul J
AU - McLaren PJ
FAU - Ball, T Blake
AU - Ball TB
FAU - Wachihi, Charles
AU - Wachihi C
FAU - Jaoko, Walter
AU - Jaoko W
FAU - Kelvin, David J
AU - Kelvin DJ
FAU - Danesh, Ali
AU - Danesh A
FAU - Kimani, Joshua
AU - Kimani J
FAU - Plummer, Francis A
AU - Plummer FA
FAU - Fowke, Keith R
AU - Fowke KR
LA - eng
GR - HOP-75348/Canadian Institutes of Health Research/Canada
GR - MDP-86721/Canadian Institutes of Health Research/Canada
PL - United States
TA - J Infect Dis
JID - 0413675
RN - 0 (Cytokines)
SB - AIM
SB - IM
MH - CD4-Positive T-Lymphocytes/*immunology/*virology
MH - Cytokines/*blood
MH - Female
MH - *Gene Expression
MH - Humans
MH - Phenotype
MH - Prostitution
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655968 [doi]
PST - ppublish
PMID- 20887220
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Determinants of protection among HIV-exposed seronegative persons: an over
view.
PG - S333-8
AB - Both clinical experience and a growing medical literature indicate that so
me
persons who have been exposed to human immunodeficiency virus (HIV) infect
ion
remain uninfected. Although in some instances this may represent good fort
une,
cohorts of uninfected persons have been reported who are considered at hig
h risk
for infection. In these cohorts a variety of characteristics have been pro
posed
as mediating protection, but to date only the 32–base pair deletion
in the
chemokine (C‐C motif) receptor 5 gene, which results in complete fa
ilure
of cell surface expression of this coreceptor, has been associated with
high‐level protection from HIV infection. With this in mind, there
are
probably many other factors that may individually or in combination provid
e some
level of protection from acquisition of HIV infection. Because some of the
se
factors are probably incompletely protective or inconsistently active,
identifying them with confidence will be difficult. Nonetheless, clarifyin
g the
determinants of protection against HIV infection is a high priority that w
ill
require careful selection of high‐risk uninfected cohorts, who shou
ld
undergo targeted studies of plausible mediators and broad screening for
unexpected determinants of protection.
AD - Center for AIDS Research, Case Western Reserve University School of Medici
ne,
University Hospitals/Case Medical Center, Cleveland, OH 44106, USA. MXL6@c
ase.edu
FAU - Lederman, Michael M
AU - Lederman MM
FAU - Alter, Galit
AU - Alter G
FAU - Daskalakis, Demetre C
AU - Daskalakis DC
FAU - Rodriguez, Benigno
AU - Rodriguez B
FAU - Sieg, Scott F
AU - Sieg SF
FAU - Hardy, Gareth
AU - Hardy G
FAU - Cho, Michael
AU - Cho M
FAU - Anthony, Donald
AU - Anthony D
FAU - Harding, Clifford
AU - Harding C
FAU - Weinberg, Aaron
AU - Weinberg A
FAU - Silverman, Robert H
AU - Silverman RH
FAU - Douek, Daniel C
AU - Douek DC
FAU - Margolis, Leonid
AU - Margolis L
FAU - Goldstein, David B
AU - Goldstein DB
FAU - Carrington, Mary
AU - Carrington M
FAU - Goedert, James J
AU - Goedert JJ
LA - eng
PT - Review
PL - United States
TA - J Infect Dis
JID - 0413675
RN - 0 (Receptors, CCR5)
RN - 0 (Receptors, HIV)
SB - AIM
SB - IM
MH - HIV Infections/*genetics/*immunology
MH - Humans
MH - Receptors, CCR5/genetics
MH - Receptors, HIV/genetics
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655967 [doi]
PST - ppublish
PMID- 20887219
OWN - NLM
STAT- MEDLINE
DA - 20101004
DCOM- 20101101
IS - 0022-1899 (Linking)
VI - 202 Suppl 3
DP - 2010 Nov 1
TI - Historical perspective on HIV-exposed seronegative individuals: has nature
done
the experiment for us?
PG - S329-32
AB - Multiple and frequent exposure to the human immunodeficiency virus (HIV) d
oes not
necessarily result in HIV infection. Approximately 15% of HIV exposed
seronegative individuals repeatedly resist infection, a phenomenon that ha
s been
observed in all investigated HIV‐exposed cohorts. This brief report
provides a limited historic perspective of the discovery of these cohorts
and
outlines some of the immunologic and genetic parameters that are associate
d with
resistance. We raise the possibility that assessing immunologic parameters
of the
phenomenon might provide insights that might be relevant for effective AID
S
vaccine design.
AD - Experimental immunology Branch, National Cancer Institute, National Instit
utes of
Health, Bethesda, Maryland, USA.
FAU - Shearer, Gene
AU - Shearer G
FAU - Clerici, Mario
AU - Clerici M
LA - eng
PT - Historical Article
PT - Research Support, N.I.H., Intramural
PT - Review
PL - United States
TA - J Infect Dis
JID - 0413675
SB - AIM
SB - IM
MH - Cohort Studies
MH - Disease Susceptibility
MH - HIV Infections/genetics/*history/*immunology/transmission
MH - History, 20th Century
MH - History, 21st Century
MH - Humans
MH - Risk Factors
EDAT- 2010/10/05 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/10/05 06:00
AID - 10.1086/655974 [doi]
PST - ppublish

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