HIV Flashcards
Where did HIV arise from?
HIV 1 - Related to simian immunodeficiency virus in chimpanzees and gorillas.
HIV 2 which is slower to progress and harder to transmit - Closely related to SIV found in other primates
Thought to have jumped species from many mechanisms including bush meat
How is HIV transmitte?
- Enters the body through mucous membranes, direct injections or via open wounds. So some activities that allow for HIV transmission are as follows:
- Anal or vaginal intercourse (oral sex isn’t efficient route)
- Injecting drugs/sharing equipment,
- Mother to child transmission
- Transmission in healthcare settings
- Transmission via donated blood/clotting factors
Explain the pathogenesis of HIV
- Infects immune cells which carry CD4 receptors such as T helper cells, macrophages and dendritic cells.
- HIV then causes depletion of CD4 T helper cells by direct killing of cells, apoptosis of uninfected cells and CD8 cytotoxic T cells killing infected CD4 cells.
- Causes abnormal B cell activation resulting in excessive immunoglobulin production.
What is the critical level of CD4 cells that increase risk of opportunistic infections?
Equal to, or below 200
What are the important HIV enzymes and some potential drug targets
Important enzymes - Integrase, protease and reverse transcriptase.
- Targers for drug treatments include: Fusion inhibitor (enfurvitide) (prevents binding to CD4 cells), nucleoside reverse transcriptase inhibitors (abacavir/tenoforvir), non-nucleoside reverse transcriptase inhibitors (efavirenz), integrase inhibitors (Dolutegravir) and protease inhibitors (Darunavir)
Describe features of HIV latency
- It is the state of reversibly non-productive infection of individual cells. This is the asymptomatic period between initial infection and advanced HIV (can be 10-15 years)
What can cause HIV drug resistance?
- Inconsistent HIV medication use.
- Infection from an HIV drug resistant strain
What are the two approaches currently being researched for an HIV vaccine
- Active vaccination which aims to induce immune response against HIV.
- Passive vaccination in which preformed antibodies against HIV are administered.
- Live attenuated vaccines are not being used ass there is risk of the HIV becoming live and infectious.
What population groups are at highest risk of contracting HIV
- Sub Saharan Africa,
- MSM,
- Children of people living with HIV,
- People who inject drugs,
- People who have transactional sex
- But really anybody
What is the method of HIV testin
4th generation testing tests for p24 antigen/HIV antibody. However has a window period of 45 days.
Can do point of care tests and can do home testing.
What are the symptoms of primary HIV infection or ‘seroconversion’
- Rash,
- Lymphadenopathy,
- Fever, weight loss,
- Malaise
- Headaches, neuropathy,
- Mouth sores and oral thrush,
- Myalgia,
- Hepatosplenomegaly,
- Nausea and vomiting
Top 4 are main ones
What are the possible differentials for primary HIV infections
- Infectious mononucleosis,
- Secondary syphilis
- Drug rash,
- Other viral infections, eg, CMV or influenza
- ALWAYS DO HIV TEST
What are some HIV indicator conditions
- Pneumocystis pneumonia,
- Oral hairy leucoplakia,
- Oesophageal candida,
- TB,
- Kaposi’s Sarcoma,
- Chronic diarrhoea,
- Bacterial pneumonia,
- Dementia,
What are the two blood markers investigated for in HIV
- HIV viral load. Undetectable is below 200 copies, in Scotland the aim is for below 20 copies/ml as this prevents transmission and improves health of patient.
- CD4. This is calculated from total lymphocyte count. There is high risk of opportunistic infection if below 200/mm cubed.
What is the treatment for HIV, its challenges and when should it be started?
- Highly active antiretroviral treatment (HAART) which should be started asap.
- This usually involves triple therapy with 2 nucleoside reverse transcriptase inhibitors and 1 drug from another class.
- Challenges include: Need for good adherence, the psychological impact the short and long term side effects and the many drug to drug interactions
What are the short and long term toxicities associated with antiretroviral treatment
Short - Rash, hypersensitivity (eps. Abacavir), CNA side effects, GI side effects, renal and hepatic toxicity.
Long term - Body shape changes (lipoatrophy, weight gain), renal toxicity with commonly used drug called tenofovir disoproxil, hepatic toxicity, lipid and bone toxicity.
What are some common drug interactions with antiretroviral therapies
It is often mediated by CYP450 enzymes. Examples of interactions include; PPIs, statins, antipsychotics, topical or inhaled drugs. So always check
Describe features of HIV partner notification and what are some HIV prevention methods
- Should be carried out by specialist HIV team.
- Prevention methods include:
- Condoms,
- Treatment as prevention (TasP)
- Pre-exposure Prophylaxis (PrEP),
- Post-exposure Prophylaxis (PEP),
- Prevention of Mother to Child Transmission (PMTCT)
- Harm reduction via needle exchange.
Describe features of PrEP/PEP (HIV - using antiretrovirals as prevention)
PEP - Is taken within 72 hours after exposure. It should be taken for 28 days and is available from sexual health/A&E.
PrEP - Available from sexual health for people at high risk of HIV through sexual transmission. Cheap and effective intervention but must emphasise condom use.
Explain some features of prevention of mother to child HIV transmission
- Transmission has fallen due to antenatal HIV screening. If mother is HIV positive then following measures are put in place:
- ARVs for mother during pregnancy,
- Minimise risk at delivery, maybe via C-section.
- PEP for baby
- Avoid breast feeding.
