HIV

Question 1

HIV

Structure:

Answer 1

similar to transposable elements

Question 2

Transposable element

Answer 2

– DNA sequence that can change position in the genome

Question 3

Transposable element

Class 1 –

Answer 3

– retrotransposons, DNA → RNA (transcription), RNA → DNA (reverse transcription)

Question 4

Transposable element

Class 2-

Answer 4

– DNA transposons, cut from genome by transposase and inserted elsewhere

Question 5

Viral retro-elements

Answer 5

-in our genome (endogenous)

Gag – capsid proteins Pol – enzymes Env – envelope proteins

Question 6

Properties

Answer 6

-enveloped, diploid RNA, lentivirus
GP – 160 composed of 120 and 41 which interacts with CD4 T cells/Macros
Core – cone shaped, capsid protein p24

Question 7

Protein synthesis: precursor genes

Gag

Answer 7

Gag – matrix, capsid (p24), and nucleocapsid proteins

Question 8

Protein synthesis: precursor genes

Pol

Answer 8

Pol – protease, reverse transcriptase, and integrase enzymes

Question 9

Protein synthesis: precursor genes

Env

Answer 9

Env – envelope, gp120 and gp41 = gp160

Question 10

Protein synthesis: precursor genes

Tat

Answer 10

Tat – activation of transcription

Question 11

Protein synthesis: precursor genes

Rev

Answer 11

Rev – regulation of RNA splicing and mRNA export

Question 12

Protein synthesis: precursor genes

Nef

Answer 12

Nef – cell activation signals, down regulates CD4, MHC1 (evasion)

Question 13

Protein synthesis: precursor genes

Vif

Answer 13

Vif – viron infectivity, required to cause disease (blocks APOBEC)

Question 14

Protein synthesis: precursor genes

Vpr

Answer 14

Vpr – G2 arrest

Question 15

Protein synthesis: precursor genes

Vpu

Answer 15

Vpu – down regulation of surface CD4, virus release, anti-BST2

Question 16

HIV

Mode of infection:

Answer 16

Receptors – Gp120 interacts with T cells/macros via CD4, CCR5 and CXCR4 – chemokine receptors
Gp41 undergoes conformational change to pull membranes together and allow fusion
Entry – partial uncoating → reverse transcriptase complex → convert RNA to dsDNA → Pre-integration complex (PIC) → enters nucleus → integrase cleaves ends and insert viral DNA into host genome
Transcription – Early – tat, rev, and nef proteins are expressed Late – structural – gag, gag-pol, env, vpu, vpr, vif
Maturation – cleavage of gag-pol with viral protease

Question 17

Innate restriction factors:

Answer 17

host proteins to handle retrovirus replication, first line defense against HIV

Question 18

Innate restriction factors:

APOBEC3

Answer 18

– G → A mutations, cytidine deaminases → incorporated into viral capsid → new virus is not infectious

Question 19

Innate restriction factors:

BST2

Answer 19

BST2 – interferon-induced membrane protein, tethers virons to plasma membrane in the absence of vpu

Question 20

Primary infection

Answer 20

– flu-like symptoms, CNS disorders, GI problems, lasts for a few weeks, high p24

Question 21

Clinical Latency

Answer 21

– asymptomatic, constant viral replication and depletion of T cells, high T cell turnover rate

Question 22

AIDS

Answer 22

<200 (A or B), opportunistic infections (C) and malignancy → death

Question 23

AIDS Dementia Complex

Answer 23

– HIV invasion of the CNS by infected monocytes/glia

Encephalitis – perivascular cuffing, giant cells, glial nodules, astrocytosis, vacuolar myelopathy

Question 24

HIV Lymphoid Interstitial pneumonitis

Answer 24

kids, alveolar macros fuse to form giant cells due to viral envelope GP

Question 25

Opportunistic infections: treated

Answer 25

prophylactically

Question 26

Opportunistic infections

Candidiasis

Answer 26

Candidiasis – CD4 T cells >200, most common fungal infection with HIV (presenting sign)

Question 27

Opportunistic infections:

Pneumocystis jiroveci

Answer 27

Pneumocystis jiroveci - <200, pneumonia with immunosuppression → TMP-SMX

Question 28

Opportunistic infections:

Toxoplasmosis, fungi

Answer 28

Toxoplasmosis, fungi - <100, undercooked meat and cat feces, CNS disease → TMP-SMX

Question 29

Opportunistic infections:

Mycobacterium

Answer 29

Mycobacterium, asperg, MAC - <50 → clarithromycin and ethambutol

Question 30

Opportunistic infections: Viral

Answer 30

Viral – CMV, EBV, HSV, JC

Question 31

Opportunistic infections: Tumors

Answer 31

Tumors – Kaposi sarcoma, NHL, cervical carcinoma (HPV), CNS lymphoma (EBV)

Question 32

Antiviral therapy:

Answer 32

inhibition of various enzymes and proteins

Question 33

Antiviral therapy:

AZT

Answer 33

AZT – thymidine analog, inhibits reverse transcriptase

Question 34

Antiviral therapy:

Protease inhibitors

Answer 34

Protease inhibitors – prevents maturation with cleavage of gag-pol → non-infectious immature virus

Question 35

Antiviral therapy:

HAART

Answer 35

HAART – combined protease and reverse transcriptase inhibitors, used when CD4<350 or with AIDS defining disease