AIDS/HIV, Molecular and Cell Biology
101
F1
F2
K
B
D
C
H
A
A2
G
J
A
F
Group M
Group N
Group O
100
100
100
0.1
CPZCAM3
CPZ.US.
CPZGAB
CPZANT
HIV-1 A
HIV-1 B
HIV-1 O
HIV-2 A
HIV-2 B
SIV
cpz
Gab1
SIV
cpz
Ant
SIV
svk
SIVsm
SIV
agm
Ver
SIV
agm
Gri
SIV
agm
Tan
SIV
mnd
SIVl
hoest
SIV
sun
0.1
(a)
(b)
Fig. 1
(a) Relationships of HIV and SIV based on
pol
sequence comparison and (b) clades
of HIV.
race in the 1930s. Within the M group,
nine clades are recognized (Fig. 1a and
b). In addition to clades, many recombi-
nant or ‘‘mosaic’’ subtypes have also been
identifed. HIV-1 and HIV-2 have a very
similar genetic structure except as detailed
be
low
.Thesequenceo±thev
irusis
,how
-
ever, very variable indeed and two clades
within the M group may di±±er in certain
regions o± the genome at the amino acid
level by 20 to 40%. This is an astonishing
level o± variation and contributes signif-
cantly to the virus’ success in establishing
in±ection in the human population.
In their native hosts, simian lentiviruses
appear to cause little disease. SIV ±rom the
A±rican green monkey, SIV
agm
,isasymp
-
tomatic in its natural host but produces
pro±ound immunodefciency when intro-
duced into rhesus macaques or cynomolo-
gus macaques. This may give us clues to
the reason why HIV is so catastrophic in
humans given the short time (
<
100 years)
that it has been in±ecting humans and
the consequent lack o± host or pathogen
adaptation.
Thenamelentivirus(lenti
=
slow) is de-
rived ±rom the archetypal member o± this
±amily, Maedi-Visna virus, which in±ects
sheep and causes a very slow progressive
disease involving pneumonic change and
wasting, sometimes associated with cen-
tral nervous system de±ects. In HIV, there
may be symptoms associated with the ini-
tial viremia but therea±ter, the speed o±
onset o± clinical disease ±ollowing in±ec-
tion is variable and in±ected individuals
may remain asymptomatic ±or a number
o± years be±ore the immunodefciency be-
comes severe enough to cause illness.
Both HIV-1 and HIV-2 in±ection lead
to
a
progressive
decline
in
immune
competence to the point where it becomes
incapable o± protecting the individual
±rom otherwise very low pathogenicity
in±ections, which are easily dealt with
by a normal individual. This progressive
loss o± immune competence has given
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