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HIV and AIDS Flashcards

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1
Q

Immunology of HIV infection

A

Virus has a surface glycoprotein which binds to CD4 glycoprotein on the surface of the host cells
The most important target for the virus is the CD4-bearing lymphocytes which the virus infects and subsequently destroys

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2
Q

What does the progressive destruction of CD4+ lymphocyte population correspond to?

A

Disease progression from HIV infection

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3
Q

What is the normal CD4 lymphocyte count?

A

500-1500 cells/mm^3

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4
Q

A patient is asymptomatic from HIV infection until the CD4 lymphocyte count is at what level?

A

< 200 cells/m^3 - below this level the patient’s risk of opportunistic infection and tumour disease rises dramatically

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5
Q

Patient signs and symptoms which indicate progression of HIV infection

A

Weight loss
Lymphadenopathy
Thrush
Skin and oral disease

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6
Q

When should patients with HIV be started on antivirals?

A

If CD4 < 350

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7
Q

When should PCP prophylaxis for HIV patients be started?

A

When CD4 < 200

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8
Q

Why should a one off cell count not form the basis for treatment of a patient with suspected HIV?

A

The absolute cell count can fall in a healthy patient with an intercurrent infection so treatment should be based on a series of results

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9
Q

What is the HIV viral load like?

A

Initially high during acute infection but usually falls to a low level, only rising again in the later stages of the disease - usually after 6-8 years of infection

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10
Q

How is the HIV viral load quantified?

A

Using PCR assay to measure the number of RNA copies per ml blood, also now used to measure patient response to antiviral treatment

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11
Q

When might a change in antivirals need to be considered?

A

If the viral load is not suppressed to < 40 copies per ml blood with current combination

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12
Q

What factors influence the disease progression of HIV?

A

Age
HLA type
History of seroconversion illness

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13
Q

Rate of progression of HIV if untreated

A

25% to early symptoms after 5 years and 50-70% to severe symptoms and opportunistic infections after 10 years if untreated

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14
Q

What receptor has been studied and is now a target for drug treatment of HIV?

A

Chemokine receptor 5 (CCR-5)

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15
Q

How do HIV infected patients with a single CCR-5 mutation respond to HIV infection compared to others?

A

Appear to have a slower rate of HIV disease progression

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16
Q

Presentation of primary HIV infection

A

Rash
Fever
Pharyngitis
Lymphadeopathy

Similar to glandular fever presentation

May also develop diarrhoea, meningitis or neuropathy

Self-limiting illness

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17
Q

Investigations to be done in primary HIV infection

A

Blood should be taken early in its course and during the convalescent period to test for HIV antibody
HIV viral load testing

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18
Q

What are the typical features of the early and late blood samples taken during a primary HIV infection?

A

Early sample will be antibody negative but antigen positive

Late sample will usually be antibody positive, but this may take up to three months to develop after the illness

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19
Q

HIV viral load testing is sufficiently sensitive to allow detection of

A

HIV during seroconversion and before the development of antibodies

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20
Q

Severe or prolonged seroconversion illness is recognised as

A

a poor prognosticator, correlating to more rapid disease progression

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21
Q

What are the two distinct virus types that HIV can be classified into, and which is more common?

A

HIV 1 and HIV 2

HIV 2 is much less common

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22
Q

Laboratory aspects of HIV infection

A

Causes persistent infection of cells

Easily inactivated by heat, drying and disinfectants

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23
Q

How do HIV 1 and 2 work?

A

Replicate via a DNA intermediate step using the viral enzyme reverse transcriptase
Conversion of RNA to DNA is an error-prone process
The errors cannot be corrected so result in virus diversity
GIV attachments to cells, reverse transcriptase and viral enzymes are all targets for HIV drugs

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24
Q

Main diagnostic method for determining whether a person is infected with HIV

A

combined test for HIV antigen and HIV antibody

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25
How long after exposure might a combined antigen and antibody test take to become positive?
Up to 3 months
26
When should a person be considered infectious?
A person positive for HIV antigen/antibody should be considered infectious, but a negative HIV antigen/antibody test does not exclude infection if there may have been exposure in the previous 3 months
27
What does HIV viral load test do?
Quantifies the amount of the virus in the blood
28
When is the viral load high?
During the window period of infection when antibody is absent
29
Main use of HIV viral load
monitor effectiveness of antiretroviral therapy
30
When are tests for viral nucleic acid used?
To diagnose infection in babies of HIV-infected women, as the passive maternal antibody can persist for 15 months, making diagnosis using HIV antigen/antibody test difficult
31
What is involved in HIV resistance testing?
Looking for specific nucleic acid changes associated with resistance to the individual antiretroviral agents, aids decision on optimal therapy
32
What led to the description of the acquired immune deficiency syndrome (AIDS)?
In 1981, two previously very rare diseases in young men in the USA - pneumonia and Kaposi's sarcoma - were noticed to be occurring in homosexual men, indicating that some sort of immunodeficiency was occurring in previously fit homosexual men
33
How may people are affected by HIV worldwide?
34 million, over 90% living in the developing world
34
How is HIV spread and what are its modes of transmission?
Spread by blood and body fluids Modes of transmission; sex blood mother-to-child
35
What is the commonest route of transmission of HIV in adults globally?
Heterosexual transmission
36
Modes of transmission relate directly to
prevention strategies for transmission Also relate to groups at high risk for HIV
37
Examples of groups of people at high risk for HIV infection
Homosexual and bisexual men IVDA Those who have had sex with someone from a high prevalence area Recipients of unscreened blood, blood products, tissue or organ (not in the UK) Sexual contact with a person at risk Child of HIV-infected mother
38
What are the risks of transmission of HIV to a healthcare worker following a significant percutaneous exposure, if no preventative action is taken?
Approximately 30% for a source positive for hepatitis B surface and E antigens 3% for a source positive for hepatitis C RNA 0.3% for a source positive for HIV
39
Are the risks of transmission greater following percutaneous or mucocutaneous exposure?
Mucocutaneous
40
What are the body fluids which should be handled with the same precaution as blood?
``` CSF Pleural, peritoneal and pericardial fluid Exudate or tissue fluid from burns or skin lesions Breast milk Amniotic fluid Vaginal secretions Semen Synovial fluid Any fluid containing visible blood Saliva ```
41
What immediate actions should be taken after blood/body fluid exposure?
Wash off splashes on skin with soap and running water Encourage bleeding if skin has been broken Wash out splashes in eyes, nose or mouth Assessment of risk of virus transmission by someone other than the victim Report the incident
42
Factors to be considered in risk assessment
Source of contamination Extent of injury and how it was caused Likelihood of hepatitis B or C or HIV in the source Hepatitis B vaccination status of the victim
43
By what percentage can combination antiretroviral therapy decrease the risk of HIV infection?
80%
44
When should combination antiretroviral therapy be started following possible exposure to HIV?
Ideally within 1 hour, but still worthwhile up to 72 hours post-exposure, generally not recommended beyond 72 hours
45
Immunisations available for Hepatitis B
Active - recombinant | Passive - hepatitis B immunoglobulin
46
Immunisations available for hepatitis C
No vaccine, immunoglobulin or antiviral therapy for post-exposure prophylaxis available
47
When testing an identified source, when should post-exposure prophylaxis for HIV (if indicated) be started?
Before the test results
48
Early diagnosis and treatment of hepatitis C is associated with
higher likelihood of cure
49
Steps to avoiding exposure to blood-borne viruses in the health care setting
Use of good hygiene practices with regular hand washing Cover existing wounds/skin lesions with waterproof dressings Take simple protective measures to avoid contamination of person and clothing Protect mucus membranes Prevent puncture wounds, cuts and abrasions in presence of blood Avoid sharps where possible Use safe procedure for sharps handling and disposal Clear up spillage of blood and body fluids promptly and disinfect contaminated surfaces Dispose of contaminated waste safely
50
When should infected pregnant women be started on therapy?
Before the third trimester
51
When is the three drug combination adjusted?
If viral load is not adequately suppressed after 4-6 weeks of therapy
52
Current life expectancy of patients diagnosed at age 20 with CDF counts of; < 100 100-200 > 200
< 100 - 52 years old 100-200 - 62 years old > 200 - 70+ years old
53
How long is HIV treatment?
Lifelong
54
Once the virus penetrates the host cell, what happens?
It releases RNA which must be converted to DNA to allow incorporation into the host genome - this process is known as reverse transcriptase
55
What was the first group of drugs with activity against HIV?
Nucleoside reverse transcriptase inhibitors - zidovudine - didanosine - zalcitabine - lamivudine - stavudine - abacavir
56
What is the possible consequence of nucleoside reverse transcriptase inhibitors therapy?
They are nucleoside analogues which interfere with the function of many healthy host cells, including marrow cells, so marrow toxicity is a frequently encountered adverse effect
57
What was the first drug to be licensed for HIV treatment?
Zidovudine
58
When is zidovudine particularly useful?
In reducing transmission of infection from mother to infant during pregnancy and in stopping the development of AIDS dementia
59
In what time would patients taking zidovudine monotherapy develop resistant strains of HIV?
Within 18 months of starting treatment
60
What class of drugs is currently used as first line treatment in combination with nucleoside analogues?
Non-nucleoside reverse transcriptase inhibitors
61
How do non-nucleoside reverse transcriptase inhibitors work?
Act on the reverse transcriptase enzyme at a different site from the nucleoside analogues, sometimes better tolerated
62
What is the commonest side effect of the non-nucleoside reverse transcriptase inhibitor efavirenz?
Vivid dreams/nightmares
63
How do protease inhibitors work?
Inhibit the virus protease enzyme which cleaves polyproteins into proteins which are required for viral maturation - most potent group of antivirals
64
Why might the benefit of protease inhibitors be short-lived if given alone?
Resistance can develop
65
What is a possible side effect of protease inhibitor use?
Raised cholesterol levels occur in many patients taking this group of drugs, can have implications for development of premature vascular disease
66
How do integrase inhibitors work?
Act by preventing viral DNA integration into the CD4+ cell chromosome
67
Give an example of an integrase inhibitor
Raltegravir
68
How do chemokine receptor antagonists work?
Act by interfering with the interaction between HIV and CCR-5
69
How do fusion inhibitors work?
Inhibit the attachment of the virus to host cells, preventing virus entry into cells and viral replications, have to be administered as injections currently
70
When do most clinicians introduce three drugs in treatment of HIV?
When patients develop symptoms or laboratory markers which suggest disease progression
71
What current techniques and development should make it possible in the future to know which drugs the virus will respond to before treatment is started and which ones it is resistant to after treatment fails?
Laboratory techniques which allow the analysis of HIV for detection of the genetic mutations associated with resistance to reverse transcriptase inhibitors or protease inhibitors
72
Why is compliance important in HIV treatment?
Poor drug compliance and intermittent dosing will promote viral resistance. Studies show that patients need to be > 95% compliant to achieve the optimum effect of their drug regime
73
Side effects of HIV drugs
``` Lipodystrophy (stavudine, AZT) Anaemia (AZT) Pancreatitis (esp didanosine) Neuropathy (esp stavudine) Hepatitis (esp nevirapine) Drug interactions (protease inhibitors and NNRTIs) ```
74
What is lipodystrophy?
Loss of subcutaneous fat from the face and limbs with redistribution to the breasts and abdomen, significantly altering the patient's appearance
75
Side effects of nucleoside reverse transcriptase inhibitors
Marrow toxicity Neuropathy Lipodystrophy
76
Side effects of non-nucleoside reverse transcriptase inhibitors
Skin rashes Hypersensitivity Drug interactions
77
Side effects of protease inhibitors
Drug interaction Diarrhoea Lipodystrophy Hyperlipidaemia
78
Side effects of integrase inhibitors
Rashes
79
Challenges of HIV care
``` Ageing population Osteoporosis Cognitive impairment Malignancy Cerebrovascular disease Renal impairment Ischaemic heart disease Diabetes mellitus ```
80
HIV prevention
``` Behaviour change Condoms Education Circumcision Treatment Pre-exposure prophylaxis Post-exposure prophylaxis for sexual exposure ```
81
Skin manifestations of HIV
``` Seborrheic dermatitis Molluscum contagiosum Shingles Recurrent varicella zoster virus Recurrent genital, perianal or oral herpes, often severe and extensive ```
82
Oral manifestations of HIV
Oral hairy leukoplakia (OHL) | Oral candidiasis
83
Tumours associated with HIV
Kaposi's sarcoma | Lymphoma
84
Features of Kaposi's sarcoma
Vascular tumour arising from endothelium Develops in multifocal way No obvious spread through blood or lymphatics Skin is commonest site, also occurs on hard palate, in gut and in bronchi
85
Cause of Kaposi's sarcoma
Herpes virus - Kaposi's associated virus (KAV)
86
Transmission of KAV
Probably sexual or through close contact
87
Treatment of Kaposi's sarcoma
Effective HIV antiviral treatment can often lead to resolution
88
Common sites of Lymphoma in HIV
B cell lymphoma at many unusual sites e.g. gut and soft tissue, cerebral lymphoma is the most commonly seen
89
Prognosis of lymphoma in HIV
Extremely poor as most patients are intolerant of chemotherapy, best approach may be to use highly active antiretroviral therapy in combination with chemotherapy
90
Features of primary HIV infection
Asymptomatic | Acute retroviral syndrome
91
Features of HIV clinical stage 1
Asymptomatic | Persistent generalised lymphadenopathy
92
Features of HIV clinical stage 2
``` Moderate unexplained weight loss, < 10% of presumed or measured body weight Recurrent RTI e.g. sinusitis, tonsillitis Herpes zoster infection Angular cheilitis Recurrent oral ulceration Papular pruritic eruptions Seborrheic dermatitis Fungal nail infections ```
93
Features of HIV clinical stage 3
Unexplained severe weight loss > 10% presumed or measured body weight Unexplained chronic diarrhoea for > 1 month Unexplained persistent fever for > 1 month Persistent oral candidiasis Oral hairy leukoplakia Pulmonary tuberculosis Severe presumed bacterial infections Acute necrotising ulcerative stomatitis, gingivitis or periodontitis Unexplained anaemia Neutropenia Chronic thrombocytopenia
94
Features of HIV clinical stage 4
``` HIV wasting syndrome Pneumocystis pneumonia Recurrent severe bacterial pneumonia Chronic HSV infection Oesophageal candidiasis Extrapulmonary TB Kaposi sarcoma Cytomegalovirus infection CNS toxoplasmosis HIV encephalopathy Cryptococcosis extrapulmonary Disseminated non-TB mycobacteria infection Progressive multifocal leukoencephalopathy Candida of the trachea, bronchi or lungs Chronic cryptosporidiosis Chronic isosporiasis Disseminated mycosis Recurrent non-typhoidal salmonella bacteraemia Lymphoma Invasive cervical carcinoma Atypical disseminated leishmaniasis Symptomatic HIV associated nephropathy/cardiomyopathy Reactivation of American trypanosomiasis ```

Infection (14 decks)

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