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Infectious Diseases and their Control > HIV > Flashcards

HIV Flashcards

1
Q

Properties of a Retro-transcribing virus (HIV)

A

Single-stranded RNA with reverse transcriptase

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2
Q

What family of viruses is HIV?

How does this family of viruses produce its DNA?

A

Retroviridae family.

Uses reverse transcriptase to produce DNA from RNA.

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3
Q

What is the Genus and subgenus of HIV?

A

Genus: Lentivirus

Subgenus: Primate Lentivirus (infects primates)

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4
Q

What is the species of HIV?

What are the two types of HIV?

A

Species: Human Immunodeficiency Virus

Types: HIV-1 and HIV-2

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5
Q

What are the symptoms of HIV?

A

Acute HIV Infection symptoms:

Systemic: Fever and weight loss. Central: Malaise, headache, neuropathy. Lymph nodes: Lymphadenopathy. Skin: Rash. Gastric: Nausea, Vomiting. Liver and spleen: Enlargement
Muscles: Myalgia Oesophagus: Sores Pharyngitis. Mouth: Sores, thrush. May get penile ulcer. Symptoms may be symptomatic: can be months to years to forever. Symptoms are variable.

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5
Q

What is AHD (Advanced HIV Disease)?

A

Used to be called Acquired Immune Deficiency Syndrome (AIDS)

Body open to opportunistic infections

Higher likelihood of cancers and systemic issues (fever etc.)

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5
Q

What are the origins of HIV-1?

A

Zoonotic infection from chimpanzees . Likely arose in western equatorial Africa . 4 major groups (M, N, O, P). Each a separate introduction into humans. Group M has 12 subtypes currently

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6
Q

Describe the structure of HIV.

A

Lipid bilayer with glycoproteins 120 and 41. P17 Matrix - a structural protein. proteases found within matrix and p24 caspid . p24 caspid containing: RNA, Integrases, p9 nuclear caspids, reverse transcriptases

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7
Q

What are the main symptoms of Advanced HIV Disease (AIDS)?

A

Central: Encephalitis, Meningitis. Eyes: Retinitis
Lungs: Pneumocystis pneumonia, Tuberculosis (multiple organs), Tumors. Skin: Tumors
Gastrointestinal: Esophagitis, Chronic Diarrhea, Tumors

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8
Q

What are the origins of HIV-2?

A

Zoonotic infection from sooty mangabeys

Likely arose in West Africa

8 known groups (A-H)

A and B most prevalent

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9
Q

Summarise the Historical Spread of HIV.

A

1950s: Retrospective analyses found HIV is African samples and from 50 Ugandan children from the 1970s

early 1970s: Small HIV outbreak in Haiti - Seems to have been the source of most non-African cases afterwards

1970s: Began spreading in USA and elsewhere.

Epidemic announced in 1982: Recognised by clusters of unusual opportunistic diseases

1982-84: Several somewhat independent discoveries of virus with multiple names
1990s: epidemic peaks, leading cause of death in 15-44 year olds in the USA by 1995.
Development of drug reigmens in mid 1990s tackles case numbers
2010: HIV counted as a chronic disease in many countries

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10
Q

What are the HIV risk groups?

A

Gay, bisexual and other men who have sex with men.
Commercial sex workers.
Intravenous drug users
Prisons
Transgendered

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11
Q

What are the ways HIV is transmitted?

A

Sexual contact: Anal (most common), vaginal, oral (extremely low but not zero). Blood-borne: Unsterilized pre-used needles, blood transfusion (90%). Mother to child: 15-30% from pregnancy/delivery, 5-20% from breast feeding. HIV needs to contact the blood for successful transmission/infection, cant pass trough epithelial cells.

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12
Q

HIV Life Cycle

A

Fusion of HIV to the host cell surface. HIV RNA, revser transcriptase, integrase and other viral proteins enter host cell. Viral DNA formed by reverse transcription. Viral DNA transcproted across nucleus and intergrates into host DNA. New viral RNA used as genomic RNA and to make viral proteins. New viral RNA and proteins move to cell surface and a new imature HIV forms. Virus is released. Vial protease cleaves new polyproteins to create mature infectious virus.

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13
Q

What does the HIV genome encode for?

A

Matrix/Caspid
Regulatory proteins
Viral enzymes
envelope

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14
Q

How is AIDS diagnosed?

A

CD4+ T-cell count
<200 cells/microlitre

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15
Q

What are the 3 forms of HIV testing?

A

Antigen: No longer recommended, low sensitivity, P24 (caspid) antigen from HIV particle, useable from 2 weeks post-infection. Antibody: most common test, used months post exposure, can have false positives which are confirmed with a Western Blot. Viral Load: not recommended, low accuracy, PCR-Based, can be used soon after exposure

16
Q

What is 4th generation HIV testing?

A

A combined antigen/antibody test.
Most common HIV test in UK
Recommended 4 weeks post exposure - detects 95% of infections

17
Q

What is the recommended test frequency for HIV?

A

High risk groups: every 3-6 months
Others: At least once

18
Q

List the types of HIV tests and what they test for.

A

PCR/Viral load: Tests for RNA/DNA (Viral genetic material)
p24 only test (Ag): Tests for Antigen
4th generation antigen/antibody tests (Architect, Duo, Combo/Combi..): Tests for antigen and antibody
1st/2nd/3rd generation tests (ELISA, EU, MEIA/ELFA/ECLIA, TriDot): Tests for antibody
Rapid Tests (Finger prick and oral swab tests (OraQuick)): Antibody
Western blot tests looking for antibodies to specific HIV proteins (confirm HIV positive antibody result): Tests for antibody

19
Q

What is HAART?

A

HIV Treatment: Highly Active Anti-retroviral Therapy. Recommended to start at diagnosis. Extremely effective.

: Turned a leading killer into a chronic disease.

20
Q

What is U=U?

A

Undetectable viral load = untransmittable HIV

21
Q

What causes HIV drug resistance?

A

Most HIV drugs target specific epitopes, so specific point mutations of HIV reduce drug effectiveness- Monotherapy not effective..
Constant drug pressure selects for viruses with point mutation, despite likely reduced fitness.

22
Q

Describe the approach to the drug treatment of HIV. (HAART)

A

HIV evades drugs well - treated with multiple drugs. Typically over 3 different drugs are used from over 2 different classes e.g 2 NRTIs with an NNRTI/ Integrase/ PI. Typically comes in a single pill.

23
Q

Describe the genetic diversity of HIV.

A

Mutates at the highest rate of any known biological entity due to reverse transcriptase. Lots of viral genetic diversity in the HIV of a singular patient- evades the immune system/ drugs very quickly if not kept under control.
HIV DNA mutations more likely in genetic hotspots containing homopolymeric nucleotide runs (repetitions of the same base.?)

24
Q

Describe the role of Reverse Transcriptase in HIV genetic diversity.

A

RT: Turns RNA genome to DNA genome. No proof-reading in RT - no function to detect mutations allowing mutations to occur in resulting DNA.

25
Q

What is the mutation rate of HIV?

A

Approx 3.4x10^-5 number of mutations per site occurs within each replication cycle . Human rate: roughly 2.5 x10^-8 per base per generation

26
Q

What makes HIV treatable?

A

It has many things ( RT, intergrate protease..) that humans do not have in their body. This makes them easy to target without causing ‘off-target effects’ on mitrochondira, cells ect.

27
Q

List the Types of HIV drugs and their functions.

A

ENTRY Inhibitors - stop HIV attaching to the host cell
fusion inhibitors- stop HIV from fusing and uncoating
RT inhibitors - NRTIS/ NNRTIs
Intergrate inhibitors - Stops HIV integration to the host genome
Protease inhibitors - stop HIV building its protease
maturation inhibitors

28
Q

What are NRTI drugs? What are their side effects/limitations?

A

NRTI drugs - Nucleoside reverse transcriptase inhibitors
Get incorporated into the DNA during reverse transcription and terminate the chain - Lack a 3’-hydroxyl group
Can have severe side effects - Interfere with mitochondrial DNA synthesis
Mutations in RT can reduce the enzymes affinity for the drug or allow for excision of incorporated drug

29
Q

What are NNRTI drugs? What are their side effects/limitations?

A

NNRTI - Non-nucleoside reverse transcriptase inhibtiors. Also interfere with RT but bind to the enzyme instead of interfering with the DNA. Stop protein domain movement – RT Enzyme can no longer bind DNA Very few side effects - RT homologues not found in humans. Resistance also occurs through mutations in RT - Change/block drug binding pocket

30
Q

What are Integrase Inhibitor drugs? What are their side effects/limitations?

A

Blocks integrase activity: Stops genome integration into host genome by Binding directly to the enzyme in multiple places. Used often to salvage patients who have RT mutations: can’t take NRTIs or NNRTIs. Well tolerated. Resistance mostly due to mutations in the integrase gene: Binding pocket of the drug in the pre-integration complex (Nucleoprotein complex consisting of viral and human proteins). Can also occur from mutations in the nef gene

31
Q

What are PI drugs? What are their side effects/limitations?

A

Protease inhibitors. Block cleavage of gag and pol precursors (Often analogues of the cleavage site) , stopping protease activity, creating a defective viral particle. Associated with lipid accumulation around neck/back. Mutations in protease (cuts up large HIV precursor proteins into smaller proteins which combine with HIVs genetic material to form new HIV virus) seem to enlarge the substrate binding pocket, creating resistance. Mutations in gag (structural protein of HIV-1/retroviruses) can also cause resistance

32
Q

What are Entry Inhibitor drugs? What are their side effects/limitations?

A

Entry Inhibitors: 3 forms: Block CD4 binding (gp120). Block fusion (gp41). Block chemokine (coreceptor) binding (gp120). co-receptor inhibitors - bind to the host protein and compete with the virion. Generally low adverse effects. Resistance occurs through mutations in gp120 or gp41 - not as recurrent/predictable as other resistance patterns, appearing to be protein structure modification rather than specific mutations.

33
Q

What are the 3 main types of Entry Inhibitors?

A

Block CD4 binding (gp120)
Block fusion (gp41)
Block chemokine (coreceptor) binding (gp120)

34
Q

What is PEP treatment? How is it carried out?

A

Post-exposure prophylaxis, anti-retroviral drug. Used when HIV is caught soon after exposure to be cleared from the body. Uncertainty about how to carry out this treatment - 2/3 drugs seem to be effective within a week of exposure. Treatment given for 4 weeks. Regular 6-12 weekly follow-ups undertaken to check for infection.

35
Q

What is PrEP treatment? How is it carried out?

A

Preventative treatments. Anti-retroviral drugs for high-risk groups. Stops HIV from taking hold in recipient. >99% effective. Must be coupled with safe sex training and regular testing.

36
Q

What is the most common drug used for PrEP?

A

Truvada: Tenovir and Emtricitabine (NRTIs) in combination

37
Q

How do vaccines work?

A

Most vaccines work by eliciting a small set of neutralising antibodies against a few viral surface proteins

38
Q

What are the difficulties in creating a HIV vaccine?

A

HIV has a very high mutation rate
Viral virions can remain dormant so its hard to target all of them
Difficult to elicit a strong antibody response without being already infected.

39
Q

Describe new attempts at a HIV vaccine.

A

Most trialled vaccines shown to be ineffective, however:

Broadly neutralising antibody VRC01 has been found to be effective against 90% of circulating strains: Binds the CD4 contact site of gp120. Only produced years post-HIV infection- Vaccine would need to elicit the production of these antibodies pre-infection

NCT05001373: mRNA-based vaccine trial. Engineered HIV envelope proteins to elicit germline B-cell responses. Only began in October 2021

Infectious Diseases and their Control (17 decks)

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