MT3 Session 16: Retroviruses Flashcards
retrovirus capsid
icosahedral or conical
Retrovirus genetic material- what type, lin/circ, how many?
+ ssRNA with trna replication primer, 2 molecules / virion
HIV classification
Group VI: +RNA retroviruses
name simple retroviruses
ALV 0 avian Leukosis virus
RSV Rous Sarcoma Virus
retrovirus life cycle
- spike protein induces CAPSID entry to cell
- reverse transcriptase and +rna is released; dsDNA ismade
- lysogeny by integrase
- make parts and BUD (NO LYSIS)
retrovirus genome
SIGNIFICANT characteristic
gag, pol, env flanked by LTR (LONG TERMINAL REPEAT)
- has poly A and 5’ cap
- many genes are superimposed -need protease to mature
structure of LTR -when do retroviruses get these?
R+U5–>integr FINISH
acute transforming retroviruses
carry viral oncogenes, oftenreplication defective
nonacute retroviruses
mechanism
activate celllular proto-oncogeneexpression
provide a promoter to c-onc, or activates a cellular promoter to c-onc
HTLV-1
unacute retrovirus,
Human T-Cell leukema Virus - encodes Tax regulatory protein
MMTV
mouse memory tumor virus
ongogenic envelope protein
RSV’s open reading frames
Rous sarcoma virus-
gag, pol, (env), src (sarcoma)
v-src
viral oncogene in rous sarcoma virus
c-src
cellular proto-oncogene in rous sarcoma virus
ITAM
immunoreceptor Tyr0based activation motif
what protein makes the LTR in retroviruses?
long terminal repeat
by reverse transcriptase
What is LTR for?
IN uses it to integrate into host DNA
RSV?
acute/nonacute? why?
defective?
acute - has src (sarcoma)
can be defective or not
ITAM
immuonreceptor Tyr-based activation motif - envelope protein - receptor in MMTV
endogenous retrovirus
doesn’t leave - don’t cause problem
retrotransposon
lost env - can’t replicate
but has RT
XMRV
xenotropic murine leukemia virus-related virus
LINE/SINE
retrovirus remnant
XMRV evidence gainst
absense in multiple
retest as -
how was XMRV made in lab?
2 endogenous retroviruses recombined to 1
within mouse
which strain of HIV is more virulent?
HIV 1
98% vs 25%
capsid structures
hexamers or pentamers
Retrovirus acessory genes
overlap
what do you need to o to get RT into cell?
have spike protein insert capsid
partial degradation of capsid
Life Cycle of HIV: attachment
- CD4 and CCR bind HIV spike protein’s TM, SU
membrane fuses
tetherin
host stops HIV1 from fleeing by tethering to cell
Vpu
cleaves tetherin in HIV
HIV theraputic targets
stop attachment by fusion inhib/CCR5 inhib
stop maturation with protease inhibitors
stop reverse transcription with NTRI and nNTRIs
NTRI = nucleoside NT inhib - 3’deoxy
NTRIs
AZT - has azido group on 3’ carbon, acyclovir
HAART
highly active anitretroviral therapy
use NTRI, nNTRI, protease inhibitors - > P(resistance)
HIV evolutionary origin
from simian immunodifficiency virus - HIV 1 and 2 independently for CHIMPANZEES
how to make retroviruses theraputic
target genes with packaging sequences
gag and pol with no packaging sequences
env with no packing sequencing
downside of using retroviral gene therapy
leukemia - nonacute
Group # of iinfluenza virus
V
orthomyxoviridae
influenza virus
influenza virus genome: #
6-8 seg
influenza virus: H
hemagglutinin : binds neuraminic acid to start infection
influenza virus: N
neuraminidase: hydrolyzes neuraminic acid to release virus
inhibitors of influenza
inhibits neuraminidase-zanamivir
why are there so many flus?
if infected with more than 1 influenza, segments can reassort
antigenic variation mechanism
antigenic drift: missense mutation
antigenic shift: segment reasortment
H5N1
highly pathogenic avian flu - from poultry
Moratorium controversy
preparedness for epidemic vs. bioterror agent.accidental release
How does influenza virus help Haemophilus influenzae?
flu attacks body - cell damage/immune response that trigger h influenza to disperse
