HIV???

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HIV (Human Immunodeficiency Virus) ???????? ?????
?????? AIDS (Acquired Immune Deficiency Syndrome)

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• HIV???
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• HIV??????????
• HIV????????
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• HIV???
• 1981 ??
• 1983 ??????HIV-1
• 1986 ???HIV-2
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• CD (cluster of differentiation 150)

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2008??????????????????????
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AIDS?????????? 1.?????????????? 2.?????????????
????? 3.??????????????EB?? 4.????????????????? 5
.????????????????? ?94??AIDS????????????? ??AIDS
????,??CD4??200 Cells/mm3
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http//www.unaids.org/en/default.asp
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FIG Number of people newly infected with HIV
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??2005??AIDS???????????????AIDS
????,??CD4??200Cells/mm3
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2455
1812
713
630
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????????????????????HIV???????
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• ?????(???????(????)?MDMA?
• ???????(FM2?K???)

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????????????? ?????? kDa
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Pprotein?????
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?? Single strand
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HIV?????????????????????
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gp120
CD4
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HIV?????

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• ELISA?????????(????)
• ?????(p24????)(????)
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• RT-PCR (??????)
• CD4CD8
• CD (cluster of differentiation 150)

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ELISA?????????
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SDS-PAGE????????? Sodium Dodecyl Sulfate
PolyAcrylamide Gel Electrophoresis
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HIV?????????????
??????? ?????? AZT (Azidothymidine)
Saquinavir ddC (Dideoxycytidine)
Ritonavir ddI (Dideoxyinosine)
Indinavir d4T (Stavudine)
Neffinavir 2TC (Lamivudine) Nevirapine Delavirdine
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Table 1. HIV ??????? HIV properties
Consequences High
variability Escape
from humoral and cellular
immunity
Infection of memory T-cells Little
target antigen expression for CTL Integration
into host cell genome Hide from the immune
system.
Permanent infection High
replication rate Rapid
seeding of newly expanded
immune
cells Infection of antigen presenting cells
Altered presentation of HIV antigens Infection
and destruction of T Blunts/alters CD8 and
B-cells immune helper cells
responses Structural
complexity of envelope Difficult targets for
neutralizing
antibodies V3 loop
variability High glycosylation of gp120
Poor accessibility of the receptor-binding site
Oligomeric arrangement Glycosylation of
gp120 epitopes Possible T-cell masking
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The cytoplasmic body component TRIM5   restricts
HIV-1 infection in Old World monkeys MATTHEW STRE
MLAU1, CHRISTOPHER M. OWENS1, MICHEL J. PERRON1,
MICHAEL KIESSLING1, PATRICK AUTISSIER2
JOSEPH SODROSKI1,3 1 Department of Cancer
Immunology and AIDS, Dana-Farber Cancer
Institute, Department of Pathology, Division of
AIDS, Harvard Medical School, Boston,
Massachusetts 02115, USA2 Division of Viral
Pathogenesis, Beth Israel Deaconess Medical
Center, Department of Medicine, Division of AIDS,
Harvard Medical School, Boston, Massachusetts
02115, USA3 Department of Immunology and
Infectious Diseases, Harvard School of Public
Health, Boston, Massachusetts 02115,
USA Correspondence and requests for materials
should be addressed to J.S. (joseph_sodroski_at_dfci.
harvard.edu).
simian immunodeficiency virus, SIV ????????
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APOBEC3G(apolipoprotein B mRNA-editing enzyme,
catalytic polypeptide-like 3G protein)
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Nature 434, 1093-1097 (28 April 2005) Massive
infection and loss of memory CD4 T cells in
multiple tissues during acute SIV
infection Joseph J. Mattapallil1, Daniel C.
Douek2, Brenna Hill2, Yoshiaki Nishimura3,
Malcolm Martin3 and Mario Roederer1 Abstract It
has recently been established that both acute
human immunodeficiency virus (HIV) and simian
immunodeficiency virus (SIV) infections are
accompanied by a dramatic and selective loss of
memory CD4 T cells predominantly from the
mucosal surfaces. The mechanism underlying this
depletion of memory CD4 T cells (that is,
T-helper cells specific to previously encountered
pathogens) has not been defined. Using highly
sensitive, quantitative polymerase chain reaction
together with precise sorting of different
subsets of CD4 T cells in various tissues, we
show that this loss is explained by a massive
infection of memory CD4 T cells by the virus.
Specifically, 30-60 of CD4 memory T cells
throughout the body are infected by SIV at the
peak of infection, and most of these infected
cells disappear within four days. Furthermore,
our data demonstrate that the depletion of memory
CD4 T cells occurs to a similar extent in all
tissues. As a consequence, over one-half of all
memory CD4 T cells in SIV-infected macaques are
destroyed directly by viral infection during the
acute phasean insult that certainly heralds
subsequent immunodeficiency. Our findings point
to the importance of reducing the cell-associated
viral load during acute infection through
therapeutic or vaccination strategies.
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HIV vaccines brief review and discussion of
future directions Karen S Slobod, Mattia
Bonsignori, Summary Expert Review of Vaccines
Jun 2005, Vol. 4, No. 3, Pages 305-313 A major
barrier to the design of a successful HIV vaccine
is virus diversity,which is particularly apparent
in the envelope glycoprotein, the target of
neutralizing antibodies. An antibody generated to
one envelope glycoprotein may not recognize an
isolate bearing a different envelope
glycoprotein. Thus, single-envelope glycoprotein
vaccines have protected against homologous but
not necessarily against heterologous challenge.
Antigenic diversity has been addressed in the
design of vaccines for other pathogens by the
preparation of polyvalent vaccines. The
poliovirus vaccine, for example, comprises three
serotypes of poliovirus, a feature that was
essential in providing full protection against
polio infection. Similarly, the authors propose
that overcoming HIV diversity is likely to
require the administration of a cocktail of
envelope glycoprotein antigens. Delivery of such
an array of envelope glycoproteins will elicit a
broad immune response that is potentially capable
of recognizing the diverse population of HIV-1
isolates. This article reviews data relevant to
the development of cocktail vaccines which have
been designed to elicit a wide range of envelope
glycoprotein-specific B- and T-cell responses.
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• http//www.cdc.gov.tw/index_info.asp?p_data_id_38
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