Virology11 Flashcards
Retroviruses are able to —— in our genome,with a genome of ——that can become —– eg.—–
Type A is (infectious/not)—— and (extracellular/intra)—–
Type B causes—– in vitro in —-
TypeC are (largest/smallest) —– eg.——
Integrate RNa DNA HIV Not infectious/ intracellular Cancer in mice Largest - lentiviruses (HIV)
HTLV-1 and HTLV2 causes —– and are grouped with —– under retroviruses
Cancer
HIV
T or F
Endogenous reroviruses are present in all cells and are not pathogenic
While exogenous are pathogenic
True
T or F
Endogenous retroviruses can’t become pathogenic
False
If they aquire certain modification they will become an infectious agent
T or F
Endo Retroviruses can’t integrate their genome in ours
False All can (eg. Integration of HTL1 ane HtL2 of the onc gene)
T or F
Cancer occurance after HiV infection is a hallmark of the disease (caused by HIV)
False
The main hallmark of HIV infection is——-
Sever immunodiffciency (T4 count drop)
T or F
Immunodifficiency caused by HIV is irreversible even if we are giving anti-retroviral treatment
False it’s reversible once we start the anti retroviral tx
SIVcpz:
SIVsm
Simian immunodiff virus (chimpanze)
Sooty mangabey
HIV 1 evolved from—— while 2 evolved from——
Most cases of HIV in africa is —- while the most spread around the world is—-
Cpz
Sm
HIV 2
HIV1
Genome of HIV1:
Envelope:
Nucleocapsid:
RT: +-
RNA virus +
2 ss copies of the same strand (reserve) not segmented as influenza
Enveloped
Unique nucleocapsid (cone shaped) (cylindrical nucleoid)
RT +
Main segments of HIV genome:
1-
2-
3-
1-gag
2-pol
3-env
Envelope proteins:
With matrix proteins
Gp120
Gp41
Rep of HIV
1- attachment of gp120 then expose more receptors for more powerful binding 2- adsoption (fusion) aka uncoating 3- DNA provirus 4- integration 5- transcription 6- full transcript or 7- genomic RNa or subgenomic(mRNA) that will form the proteins 8- viral protease gag-pol 9- virus ready to be released
1-Env proteins+ bunding site:
2- co Receptors:
3- protein that will allow fusion
1-SU : gp120 (bind to cd4 on T4, macrophages dendritic cells and astrocytes) and TM (transmembrane gp41)
2- expressed after binding of gp120: those are CCR5 and CXCR4
3- gp41
Pol gene will give 3 proteins list them
PR for protease
RT for reverse transcriptase ( RNA by RT will become ssDNA, double helix of DNA and RNA , RNAse activity then polymerase activity and it will become a dsDNA be taken to nucleus)
IN for integrase ( integrate ds DNA, let it become a provirus)
Gag gene will give 4 proteins list 2 of them:
MA (matrix p17)
CA (capsid p24)
LTRs in the genome are responsible for the —— and will attract the —– for ——
And even if this part of DNa is not active it will become active.
Attacment of this genome to the host genome
Host cell machinery
Transcription (act as promotor)
T or F
Rev, tat, vpr vif vpu nef are found in all retroviruses
False only in HIV
Tat:
Role of tat:
Other genes(eg. Rev,vpr) role:
Transactivator
Activates the expression (amplification of the transcription)
Downregulation of CD4 receptor count on surface of cell (inrocognizable by immune system)
T or F
Once the integration of Viral DNA happens it will stay forever
T (persistent infection)
T or F
Antiretroviral tx can help against the latency of the virus
False
T or F
HIV causes immune dysregulation presented by anergy before immunosuppresion
True
MOT of HIV
1-
2-
3-
Sexual relations (penetrative or not)
Contaminated blood
Transplacentally
The most efficient transmission of HIV is thru—–
Direct blood
Why MSM has a higher risk of getting infected with HIV?
Because usually during anal sex the rectum is not lubricated as the vagina which will predispose it to microscopic cuts that will transmit the HIV
Why oral sex have lower risk of infection with HIV?
Because usually saliva kills HIV virus unless the reciever has a dental extract or a small cut.
T or F
Sexual or any body fluid on a wound will have 60% risk of infection
False
100% will be infected
T or F
Risk of getting HIV without presence of wounds is 13%
False
0.5-3 (awal she helu byehke l dr)
Steps of infection:
1- primary infection
2- dissemenation to the nearest LN then to all LN in a latent phase inside the T4 or macrophages (this stage is the first in case of blood transfusion)
3- clinical latency (2-10 years) (if i do elisa or pcr i should detect it) ( the virus is killing T4 slowly)
4- elevated expression of HIV
5- clinical disease ( production cycle of viral replication)
T or F
The risk of women getting HIV from a HIV+ man is higher than a man getting HIV from HIV positve woman
Yesss
Because vagina have mucosa(more dendritic cells but not more than that in rectumi.e MSM is more risky) while the penis is covered by skin.
All cases can be solved by remembering this anatomy
Highest risk of getting HIV is between—— while the lowest is ——- but the full risk is ——
Man to man
Woman to woman
Through blood
T or F
Uncircumsised males have lower risk of getting HiV
False
Higher because they have more mucosal cells
T or F
We can easily recognize the primary infection of HIV from EBV and CMV
False
It’s hard
After 2 months of infection CD4 count will—– while that of viral load will—– till —–(number)
T4 count will decrease till —– this is the depletion of T4
Below—– this is AIDS (aydez)
Decrease Increase 10^8 300-500 200
CMV can cause —— in AIDs stage
Candida can cause——
Herpes can cause——
Retinitis
Esophageal candida
Esophageal ulcers
Case of the man with anal ulcer with HIV but taking his medication 🥹
We treat him as a normal patient
It’s mostly the case of dehydration and constipation
Stage 3 of HIV infection have a T4 count of ——– with a clinical evidence of ——
200
Documentation of AIDs defining conditions or indicators (eshya khasa bas bl HIV)
T or F Seborrhoeic dermatitis Angular chelitis Papular pruritic eruptions Fungal nail infection Are found in HIV patients always
False
