CASE 6 - HIV/HEPATITIS Flashcards
1
Q
Name the 2 types of HIV and the patients they affect
A
HIV-1 worldwide pandemic, ~36 million people
HIV-2 West Africa/Europe, 1-2 million people, generally slower progression than HIV-1
2
Q
Name the family and viral characteristics of HIV
A
FAMILY: retroviridae
CHARACTERISTICS: ssRNA transcribed to double-stranded DNA by reverse transcriptase
3
Q
Name the antigen that is essential for HIV cell attachment
A
gp120
4
Q
Describe the life cycle of HIV
A
- HIV gp120 binds to a CD4 receptor on CD4 cell AND a co-receptor
- Fusion and release of genetic material
- HIV ssRNA transcribed to dsDNA by reverse transcriptase enzyme
- Once it becomes dsDNA, it is integrated into the host by integrase
- This T cell/CD4 cell basically just becomes a factory for more and more HIV RNA through normal cellular processes
- HIV virion assembled and released
5
Q
How is HIV transmitted?
A
- Mucous membranes/blood/tissue (below the skin) being exposed to INFECTED BODILY FLUIDS (e.g. blood, semen, vaginal fluid, breast milk)
- Mother to child transmission (particularly during delivery)
Sexual transmission most common
It is NOT transmitted through direct contact (e.g. hugging, kissing, sharing cutlery) or droplets or airborne
6
Q
Name 5 factors that increase risk of HIV transmission
A
HIGH VIRAL LOAD in the source (most important)
Concurrent STI (e.g. syphilis) - mucous membranes exposed, easier for HIV to gain access
Bleeding or gential/rectal trauma
Drug use
More sexual partners
7
Q
What type of immunity is most important when responding to HIV?
A
Cell-mediated
8
Q
HIV subverts the immune system in the following ways:
- Infects CD4 cells that control normal immune response
- Integrates into host DNA
- High rate of mutation (moving target)
- Hides in ‘immune-privileged’ tissues
- Induces a cytokine environment that the virus uses to its own replication advantage
Explain how each strategy makes it more difficult for the immune system to fight it.
A
- Infects CD4 cells that control normal immune response: impairs immune function, facilitates opportunistic infections and the development of malignancies.
- Integrates into host DNA: difficult for immune system to recognise it.
- High rate of mutation (moving target): when HIV is recognised and wiped out, the other ones that have mutated and present a different antigen will NOT be targeted.
- Hides in ‘immune-privileged’ tissues: e.g. brain, bone marrow, reproductive organs where immune cells don’t routinely enter.
- Induces a cytokine environment that the virus uses to its own replication advantage: changes the regulation of the immune system by invading CD4 cells, using it to replicate themselves.
9
Q
The precipitous, massive, and concealed depletion of CD4 cells causes impaired ability to…
(2 things)
A
- Recognise new infections/antigens
- Maintain immune memory responses (i.e. old infections that the host once developed immunity against will still infect them)
10
Q
Looking at a graph of the natural history of HIV, explain what is being shown by the two different lines
(google an image)
A
- Depletion of CD4 cells in the first 4 weeks
- Acute HIV syndrome as large-scale dissemination of the virus occurs
A small recovery of the CD4 count corresponds with a period of clinical latency (lasts anywhere from a few years to decades) as the viral load drops.
CRITICAL POINT REACHED: CD4 count becomes low enough that the person develops infections and malignancies
11
Q
An estimated __ to __% of people remain asymptomatic / unaware that they have contracted HIV
A
An estimated 10 to 60% of people remain asymptomatic / unaware that they have contracted HIV
12
Q
Are there any specific HIV symptoms?
A
NO
13
Q
What is HIV seroconversion illness / acute retroviral syndrome and when does it typically manifest?
A
Seroconversion = body producing antibodies in response to the virus.
SYMPTOMS TYPICALLY OCCUR WITHIN A MONTH OF INFECTION
It is not always accompanied by a flu-like illness, but this is a possibility.
14
Q
What are the symptoms of acute retroviral syndrome / seroconversion illness?
A
Fever, lethargy, malaise, fatigue Myalgia, arthralgia Headache Lymphadenopathy Maculopapular rash Pharyngitis Anorexia/nausea/vomiting/weight loss
15
Q
When primary HIV infection resolves, the body enters a period known as…?
A
Clinical latency
16
Q
Outline the diagnostic approach to HIV, including:
- Screening test
- Confirmatory test
- Detection of viral RNA
A
- Screening test: 4th-generation antibody-antigen test which detects antibodies and HIV antigen (p24 viral core protein) - becomes positive 2-6 weeks after exposure
- Confirmatory test: HIV-1/HIV-2 antibody differentiation immunoassay (first-choice confirmatory test). Can detect both HIV-1 and HIV-2 in ∼20 minutes.
- Detection of viral RNA: detects HIV RNA in serum or plasma and can quantify the number of copies
17
Q
List 3 advantages of the 4th-generation antibody-antigen test
A
- High specificity and a sensitivity of almost 100%
- Quicker identification of HIV infection since it looks for the p24 antigen (which appears before antibodies do)
- Can detect HIV as soon as 1 month after infection
18
Q
Which of the following can be detected the soonest?
- p24 antigen
- RNA
- Antibodies
A
RNA
Followed by p24 antigen and then antibodies
(look up image of HIV window period)
19
Q
What is a normal CD4 count?
A
500-2000
20
Q
Name 2 opportunistic infections or malignancies that occur at each of the following CD4 counts:
CD4 cell count 200-500
CD4 cell count 50-200
CD4 cell count <50
A
CD4 cell count 200-500:
Herpes zoster, pneumococcal pneumonia, oral candidiasis, TB
CD4 cell count 50-200:
non-Hodgkin’s lymphoma, kaposi sarcoma (classical tumour associated w/HIV), primary CNS lymphoma, CNS toxoplasmosis, PJP
CD4 cell count <50: disseminated MAC, CMV retinitis, cryptosporidiosis
21
Q
The WHO classifies individuals with confirmed HIV infection according to clinical features and diagnostic findings. Give an example of a findings that belongs in each of the following categories
- Primary HIV infection
- Clinical stage 1
- Clinical stage 2
- Clinical stage 3
- Clinical stage 4
A
- Primary HIV infection: acute retroviral syndrome or asymptomatic
- Clinical stage 1: persistent generalised lymphadenopathy (PGL) or asymptomatic
- Clinical stage 2: unexplained moderate weight loss (<10%), recurrent bacterial/viral/fungal infections
- Clinical stage 3: unexplained severe weight loss (>10%), recurrent bacterial/viral/fungal infections, unexplained anaemia, unexplained neutropenia, unexplained persistent fevers, unexplained chronic diarrhoea (>1 month), chronic thrombocytopenia
- Clinical stage 4: AIDS-defining conditions (e.g. kaposi sarcoma, pneumocystitis pneumonia)
22
Q
A patient presents with chronic thrombocytopenia, unexplained chronic diarrhoea, and unexplained anaemia. 4th-generation antibody-antigen testing reveals that they are HIV-positive.
What clinical stage of HIV infection is this typical of?
A
Clinical stage 3
23
Q
A patient presents with kaposi sarcoma. 4th-generation antibody-antigen testing reveals that they are HIV-positive.
What clinical stage of HIV infection is this typical of?
A
Clinical stage 4
24
Q
Name 5 risk factors for HIV
A
MSM (men who have sex with men)
Occupational exposure (e.g. DASA)
IVDU
Coming from a country w/high HIV burden (e.g. south-east asian, africa)
Vertical transmission (mother-to-child)
25
Why is it not feasible to only test for the p24 antigen?
p24 rises rapidly (~2 weeks in), but also falls as the body mounts an immune response.
This means you have to get tested very early on in the disease, which is difficult because there may be no symptoms
26
MPPD sexual history osce stuff
.
27
Is it likely for HIV to be contracted after one sexual encounter?
no
28
For which patient groups is HIV pre-exposure prophylaxis (PrEP) recommended?
Men who have sex with men
Transgender and gender-diverse people
People who inject drugs
Heterosexual men and women with a HIV-positive partner
(there are guidelines for each group based on high vs. medium risk factors. look @ ETG)
29
What is involved in PEP?
Take with 72 hours of exposure
28-day course of a 2-drug or 3-drug regimen
Come back for checkups after 1 month, 3 months, and 6 months
30
What are the indications for HIV post-exposure prophylaxis? (PEP)
3 scenarios
- Injury with HIV-contaminated needles or instruments
- Contamination of open wounds or mucous membranes with HIV-infected fluids
- Unprotected sexual activity with a known or potentially HIV-infected person
31
When should HIV post-exposure prophylaxis (PEP) be initiated?
How long is it taken for?
As soon as ideally possible (ideally within 2 hours of exposure)
GUIDELINES:
- Within 72 hours of high-risk exposure
- Taken for 28 days
32
State the route of transmission for Hepatitis A, Hepatitis B, and Hepatitis C
Hepatitis A: Faecal-oral, person-person (e.g. contaminated food or water, household contacts, MSM)
Hepatitis B: Parenteral (e.g. blood, genital secretions), sexual, perinatal
Hepatitis C: Parenteral (intranasal cocaine use is a RF)
33
State the likelihood of progression to chronic liver disease for Hepatitis A, Hepatitis B, and Hepatitis C
Hepatitis A: Never
Hepatitis B: ~10%
Hepatitis C: ~80%
When it comes to viral hepatitis
When it come to viral hepatitis, vowels (A and E) cause only AcutE hepatitis while Consonants (B, C, and D) may have Chronic sequelae as well.
34
TRUE OR FALSE? Humans are the only reservoir for Hepatitis A
TRUE
35
State the following information for HEPATITIS A:
- Incubation period (& average)
- Vaccine available?
- Prevention
- Site of replication
- Symptoms
- Incubation period (& average): 2-6 weeks, with an average of 28 days
- Vaccine available? YES
- Prevention: Vaccine, clean drinking water
- Site of replication: GIT
- Symptoms: fever, jaundice, vomiting, diarrhoea. Usually prodromal symptoms of fever + malaise, THEN jaundice.
36
Who is more likely to have symptoms of hepatitis A?
Adults
| Symptoms are rare in children <5
37
Can you transmit Hep A infection before you are symptomatic?
What is the infectiousness period?
YES - can be shed in stool 2-3 weeks before symptoms
Infectious 2-3 weeks prior to symptom onset and 1 week after.
38
TRUE OR FALSE? After contracting Hep A, you develop robust immunity.
TRUE
39
Which finding on a LFT would indicate Hep A?
Very high ALT (in the thousands)
40
ALT > AST indicates...
VIRAL HEPATITIS
41
AST > ALT indicates...
ALCOHOLIC LIVER DISEASE
42
Which diagnostic tests are used for HAV in the following situations:
- Testing for recent or current infection
- Testing for past infection
- Testing for recent or current infection: IgM antibody
| - Testing for past infection/immunity: IgG antibody
43
State the following information for HEPATITIS B:
- Incubation period
- Vaccine available?
- Prevention
- Site of replication
- Symptoms
- Incubation period: 1-6 months
- Vaccine available? YES
- Prevention: immunisation, avoiding risky behaviour (e.g. IVDU, sharing sharps, unprotected sex), screening in vulnerable populations
- Site of replication: liver
- Symptoms: many times it can be asymptomatic. Risk is that it's a silent killer --> then present with advanced liver disease.
WHEN SYMPTOMATIC: fever, rash, arthralgia, myalgia, fatigue, nausea, anorexia, jaundice, RUQ pain
Very treatable disease, but you need to detect it (tricky part)
44
Can hepatitis B cause hepatocellular carcinoma (HCC)?
YES - it is an oncogenic virus
45
In which age group is the risk of HBV-related chronic liver disease highest?
Younger populations
The younger you are when you get Hep B, the more likely it is to become chronic HBV infection (--> chronic liver disease --> cirrhosis --> HCC or liver failure)
46
HBV isolated core antigens (HBcAg) are not routinely checked in clinical practice.
When would you test for HBV core antigens?
When there will be immunosuppression (e.g. chemotherapy, organ transplantation)
Because there's a chance that it will become reactivated - the cccDNA remains in the liver, but does not circulate in blood
47
Which of the HBV markers (HBsAg, HBcAg, HBeAg, HBV DNA, Anti-HBS) would be positive and negative in the following situations:
- HBV infection
- HBV resolved infection
- Immunity
- HBV infection: HBsAg positive (HBV SURFACE ANTIGEN IS IMPORTANT IN ACTIVE INFECTION), Anti-HBcAg positive (IgM in acute, IgG in chronic), HBV DNA positive, Anti-HBS positive (Surface antibody).
- HBV resolved infection: Anti-HBS and Anti-HBc IgG, HBsAg and HBV DNA negative
- Immunity: everything negative except for Anti-HBS
look there was a good table in the lecture
https://www.youtube.com/watch?v=eocRM7MhF68 (good osmosis vid)
48
Which factors assist Hep B in persisting as a chronic infection? (Name 3)
- Integrates into host DNA
- High mutation rate
- Antiviral therapy doesn't target cccDNA
49
How does Hep B cause liver disease?
The virus itself is not hepatotoxic. Liver damage comes from the immune response.
1. Foreign virus
2. Immune activation
3. Inflammation and necrosis of liver due to immune reaction
4. Inflammation and necrosis --> liver disease
50
Which types of hepatitis are transmitted via the faecal-oral route?
Vowels (A and E) are bowels (transmitted fecal-orally) and usually only cause AcutE hepatitis
51
Give 3 examples of parenteral transmission
Contact w/infected blood:
- Shared needles
- Occupational exposure (e.g. needlestick injury)
- Blood transfusion
- Organ transplant
- Tattoos, piercings
52
Risk factors for progressive fibrosis in Hep B include:
1. Host factors
2. Viral factors
3. Environmental factors
Name 2 risk factors that belong in each category
1. Host factors: older, male, immunocompromised
2. Viral factors: having genotype C, high HBV DNA
3. Environmental factors: concurrent infections (HCV, HIV), alcohol, smoking, diabetes, obesity
53
What are the 4 possible outcomes of acute infection with HBV?
(good flow chart in Robbins)
1. Subclinical disease
2. Acute hepatitis
3. Chronic hepatitis
4. Carrier
54
Is current HBV anti-viral therapy curative?
NO - doesn't target cccDNA
Helps control the disease and hopefully:
- Prevent progression to HCC
- Prevent vertical transmission
55
HBV SUMMARY
There are acute and chronic infections
Risk of liver disease, cirrhosis, and liver cancer
Antiviral therapy does not eradicate cccDNA
56
State the following information for HEPATITIS C:
- Incubation period
- Vaccine available?
- Prevention
- Site of replication
- Symptoms
- Incubation period: 2 weeks - 6 months
- Vaccine available? NO
- Prevention: in Australia, highly prevalent amongst IVDU. Prevention = needle exchange programs, TREATMENT AS PREVENTION (esp in vulnerable populations, e.g. homeless). Safe sex.
- Site of replication: liver
- Symptoms: mostly asymptomatic (80%).
When symptomatic: acute viral hepatitis (fever, malaise, arthralgia, myalgia, RUG pain, hepatomegaly, jaundice, pruritus, nausea, vomiting, diarrhoea.
57
Is Hepatitis C curable?
YES
Newer tablets also act against all different strains of Hep C
58
How is hepatitis C diagnosed?
1. HCV antibody (IF POSITIVE: do more testing)
2. HCV RNA (maker of active infection)
If HCV RNA is detected --> treatment
59
What are the possible outcomes of acute hepatitis C infection?
1. Resolution ~15%
| 2. CHRONIC hepatitis (more common in adults, unlike in hepatitis B) ~85%
60
What are the possible outcomes of HBC-related chronic hepatitis?
Cirrhosis --> HCC
Cirrhosis --> Stable cirrhosis
Lymphotropism --> lymphoma
61
What is the first-line Hep C treatment regime in Australia?
Direct-acting antiviral drugs for hepatitis C are highly effective and well tolerated.
Sofosbuvir + Velpatasvir (1 oral combined tablet), 12 weeks. Epculsa.
Glecaprevir + Pibrentasvir (3 tablets once daily), 8 or 12 weeks (depending if there's cirrhosis). Maviret.
62
What factors affect the type of antiviral treatment for HCV?
- Cirrhosis
- HCV genotype and subtype (less relevant now)
- Prior treatment Hx
- Comorbidities
- Other medications (possible interactions)
63
What is the target population for HCV treatment?
Intravenous drug users
64
When is someone defined as cured of HCV?
Negative HCV RNA 12 weeks AFTER treatment ends
65
What is the most common cause of hepatitis?
Viruses
66
What is the first-line treatment for HIV?
Antiviral therapy:
2x nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)
1x Integrase strand transfer inhibitor (INSTI).
e.g. dolutegravir+abacavir+lamivudine (Triumeq)
67
What should be monitored in patients undergoing anti-retroviral therapy for HIV? (many things)
1. Treatment adherence
2. HIV viral load
3. CD4 count
4. Toxicity of antiretroviral therapy (CBC, EUC, LFTs, biochem)
5. RFs for CVD
6. RFs for osteoporosis
7. Screen for cancers
8. Mental health
9. Respiratory infections
68
What should be checked before taking PrEP?
- Baseline testing (HIV, HBV, HCV, pregnancy, STIs, kidney function)
- Advice on reducing risk of STIs and HIV
- Ensure the patient can attend regular follow-up
69
What should patients be counselled on prior to HIV testing?
- If they do test positive, they will need to notify previous sexual partners (this can also be done via an anonymous text)
- Agrees to be tested on the basis of understanding the HIV testing procedures, the reasons for testing and is able to assess the personal implications.
(look at the document steph sent)
70
What is the 'window period'? for HIV?
Period after which it is certain that the person being tested for an infection will not seroconvert following exposure to that infection
Officially quoted as 3 months, but most people seroconvert within 6 weeks
71
List 3 side effects of anti-retroviral therapy
- Headache
- Diarrhoea
- Lipodystrophy
(note: most adverse effects are common and short-lived)
72
Outline the management of suspected or confirmed exposure to HIV
(according to eTG)
1. If the source is HIV antibody/antigen negative and unlikely to be in the window period, no further follow-up testing of the source or exposed person is required
2. HIV antibody/antigen test at baseline, then at 4-6 weeks
3. If PEP is prescribed, re-test at 3 months
73
What criteria must be met before someone is defined as having AIDS?
EITHER:
Acquiring an AIDS-defining illness (e.g. kaposi sarcoma, pneumocystitis pneumonia, cerebral toxoplasmosis, primary lymphoma of the brain)
OR
CD4 Cell count of <200 per microlitre of blood
74
What is the goal of anti-retroviral therapy?
- Slow HIV replication
| - Help the immune system recover and fight other infections
75
List 3 things that can raise Alk Phos (ALP)
1. Pregnancy
2. Cholestasis
3. Bone growth (e.g. paget's disease, blastic cancers - prostate, breast)
76
List 2 things that can raise GGT.
GGT can be used in conjunction with ALP to distinguish between...?
1. Cholestasis
2. Alcohol
Bone growth does NOT cause GGT elevation, so it is a helpful distinguishing feature.
High ALP + Low GGT = not liver-related
77
When do AST and ALT levels rise?
Which one has low specificity for the liver?
Are they indicators of acute or chronic injury?
Liver damage
They are markers of hepatic inflammation
AST (also found in bones) has low specificity for the liver. ALT has HIGH specificity for the liver). Both are only good indicators of recent injury.
78
Why is albumin a useful marker of chronic hepatocellulr injury?
Has a 20-day half-life
79
GGT levels are found to be raised. How can it be distinguished from alcohol-related pathology vs. cholestasis?
In cholestasis, bilirubin and ALP will also be raised
80
INR is both an acute AND chronic marker of liver disease. Raised INR indicates...?
Longer clotting time
High INR = Takes longer to clot
81
Why is INR so sensitive to the liver?
Depends on many proteins that are synthesised by the liver
82
Why is chlamydia routinely tested for?
It is very COMMON and ASYMPTOMATIC
| 1 in 20 young people have chlamydia and ~75% don't know they have it
83
Which groups are at risk of contracting gonorrhoea?
- MSM
- Young Aboriginal and Torres Strait Islander persons
- Returned travellers
84
Why is it important to do an MC&S for gonorrhoea?
Resistance is emerging: need to check sensitivity via MC&S
85
What percentage of women vs. men are asymptomatic when it comes to gonorrhoea?
~80% of women are asymptomatic
| ~10% of men are asymptomatic (typically will have discharge)
86
How is PID diagnosed? Why?
Clinically; the cause is POLYMICROBIAL. In 70% of causes, no causative agent is identified.
Hence, waiting for swabs will not affect management
87
Who is at risk of syphilis infection?
- MSM
- Gender diverse
- Aboriginal and Torrens Strait Islander persons
- IVDU
- Multiple sexual partners
- Sex overseas
- Pregnant persons
Anyone with a partner who fits the above criteria
88
Why is syphilis known as the 'great mimicker'?
Signs & symptoms are similar to so many other infectious diseases
Buzz words: palmoplantar rash, maculopapular rash, patchy alopecia, snail trail ulcers in mouth, warty growths
89
Epidemiology for female and male HIV patients in Australia vs. worldwide
Australia: 90% men, 10% women
Worldwide: ~56% women
90
When would the Hepatitis B surface antigen (HBsAg) be raised?
What is the corresponding antibody, and when would this be detectable?
Acute & chronic infection
Corresponding antibody: Anti-HBS. Present 1-3 months after infection or vaccination. Presence indicates immunity
91
When would the Hepatitis B CORE antigen (HBcAg) be raised?
Trick question: HBcAg is not routinely measured in clinical practice because HBcAg forms the nucleocapsid of the virus particle, which lies beneath the viral surface. So HBcAg circulates as a part of the virus but is covered by the HBsAg. It does not circulate as a free protein in significant quantity in the blood.
92
What are the corresponding HBcAg (Hep B core antigen) antibodies? When do they appear?
Anti-HBc IgM: indicates recent infection (<6 months)
| Anti-HBc IgG: chronic or resolved infection
93
When would the Hepatitis B envelope antigen (HBeAg) be raised?
What is the corresponding antibody? What do these things indicate?
HBeAg indicates active viral replication and HIGH TRANSMISSIBILITY (can be found in acute and chronic infection)
Corresponding antibody: Anti-HBe. Indicates long-term clearance and therefore low transmissibility.
HBEAg indicates highly Enfectious.
https://www.youtube.com/watch?v=h_9EBVPADNE
94
Outline the testing algorithm for HBV
1. Screening: HBsAg + Anti-HBc IgM
| 2. If HBsAg is positive, measure HBeAg and HBV DNA to determine transmissibility
95
This is a characteristic sign of HIV seroconversion illness that can be found in the mouth.
Painful mucocutaneous ulceration
96
Who is more likely to experience symptoms of EBV; adults or children?
Adults
97
How do EBV symptoms differ from HIV?
EBV: cervical lymphadenopathy. HIV: generalised contender lymphadenopathy.
EBV: maculopapular rash that occurs after treatment with aminopenicillins. HIV: generalised rash.
EBV: possible abdo pain, jaundice & hepatosplenomegaly. HIV: none of the above (but can have other GIT symptoms such as nausea and vomiting)
EBV: tonsilitis and/or pharyngitis. HIV: painful mucocutaneous ulcerations.
HIV: myalgia, arthralgia, headache.
98
Why does viral hepatitis cause jaundice?
Liver damage causes the following to occur:
1. Hepatocytes lose the ability to conjugate bilirubin; UCB leaks into the blood.
2. Hepatocytes line the bile duct, so when they die, it also allows bile to leak into the blood (containing conjugated bilirubin).
The presence of conjugated and UCB leads to jaundice.
99
What is Hoagland's sign? Which condition can it be found in?
Bilateral upper-eyelid oedema.
An early and transient sign of EBV infection/infectious mononucleosis/glandular fever.
100
What is HAART?
Highly-active antiretroviral therapy
A combination of 3 or more antiretroviral drugs used to treat HIV.
101
What is HIV wasting syndrome?
Unwanted weight loss of more than 10 percent of a person's body weight, with either diarrhea or weakness and fever that have lasted at least 30 days.
102
What is the treatment regime for chronic hepatitis B?
1. Pegylated interferon
Good: No resistance, finite duration of therapy
Bad: Less well tolerated due to side-effect profile, only moderate antiviral activity
1. Nucleoside (Lamivudine, Entecavir) and Nucleotide (Tenofovir) analogues
Good: Potent antiviral effects, few side-effects
Bad: Risk of resistance with some drugs
103
TRUE OR FALSE? Clinically-significant infection with MAC is uncommon except among people with T-cell immunodeficiency due to AIDS, and immunosuppression resulting from treatment for transplant rejection or autoimmune diseases.
TRUE
MAC/Mycobacterium Avium Complex is caused by two types of bacteria: Mycobacterium avium and Mycobacterium intracellulare. It gains entry via respiratory or GIT epithelium.
104
Which drug classes are used for first-line HIV antiretroviral therapy?
Two nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)
+
An integrase strand transfer inhibitor (INSTI)
105
How do we test for Hepatitis B?
| Screening & follow-up if positive
SCREENING:
- HBsAg (for active infection)
- HBcAg (for previous infection)
IF POSITIVE:
- HBeAg (E antigen found in actively replication cells - gives an indication of HOW INFECTIVE they are)
- HBV DNA (viral load)
106
Which aspect of the hepatitis B virus is used in the vaccine?
Hepatitis B surface antigen (HBsAg)
107
Why might someone who has just received a HBV vaccine test positive in a screening test?
Hepatitis B surface antigen (HBsAg) is used in the vaccine
