HIV Flashcards

1
Q

WHO Clinical Staging of HIV/AIDS for adults and adolescents with confirmed HIV Infection - Stage 1

A

Asymptomatic
Persistent generalized lymphadenopathy

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2
Q

WHO Clinical Staging of HIV/AIDS for adults and adolescents with confirmed HIV Infection - Stage 2

A

• Unexplained moderate weight loss(<10% of presumed or measured body weight)
• Recurrent respiratory tract infections (sinusitis, tonsillitis, otitis media and pharyngitis)
• Herpes Zoster
• Angular Cheilitis
• Recurrent oral ulceration
• Pruritic popular eruption
• Seborrhoeic dermatitis
• Fungal nail infections

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3
Q

WHO Clinical Staging of HIV/AIDS for adults and adolescents with confirmed HIV Infection - Stage 3

A

• Unexplained severe weight loss (>10% of presumed or measured body weight)
• Unexplained chronic Diarrhoea for longer than one month
• Unexplained persistent fever (above 37.5C intermittent or constant, for longer than one month)
• Persistent oral candidiasis
• Oral hairy leukoplakia
• Pulmonary TB
• Severe bacterial infections ( eg. Pneumonia, empyrean, pyomyositis, bone or joint infection, meningitis, bacteremia)
• Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
• Unexplained anemia (<8g/dl), neutropenia (<0.5 x 10^9 per liter) and/or chronic theombocytopenia (<50 x 10 ^9 per liter)

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4
Q

WHO Clinical Staging of HIV/AIDS for adults and adolescents with confirmed HIV Infection - Stage 4a

A

• HIV wasting syndrome
• Pneumocystis pneumonia
• Recurrent severe bacterial pneumonia
• Chronic herpes simplex infection ( orolabial, genital or anorectal of more than one month’s duration or visceral at any site)
• Oesophageal candidiasis (or candidiasis of trachea, bronchi or lungs)
• Extrapulmonary TB
• Kaposi sarcoma
• CMV infection (retinitis or infection of other organs)
• CNS Toxoplasmosis

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5
Q

WHO Clinical Staging of HIV/AIDS for adults and adolescents with confirmed HIV Infection - Stage 4b

A

• HIV encephalopathy
• Extrapulmonary cryptococcis including meningitis
• Disseminated non-tuberculous mycobacterial infection
• Chronic cryptosporidiosis
• Chronic isoporidiasis
• Disseminated Nicosia ( Extrapulmonary histoplasmosis or coccidiomycosis)
• Recurrent septicemia (including non-typhoidal Salmonella)
• Lymphoma (cerebral or B-cell non-Hodgkin)
• Invasive cervical carcinoma
• Atypical disseminated leishmaniasis
• HIV associated nephropathy or HIV associated cardiomyopathy

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6
Q

When does Western Blot show indeterminate results?

A

• Early HIV infection
• HIV-2 infection
• Influenza vaccine
• Autoimmune Disease
• Pregnancy
• recent tetanus toxoid administration.

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7
Q

When is HIV rapid antibody test done?

A

• Occupational exposure
• Pregnant women presenting in labor with no previous HIV testing
• Patients who are unlikely to return for results of HIV test

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8
Q

Conditions that require urgent ART

A

• Pregnancy
• AIDS - defining conditions, including HIV-associated dementia and AIDS - associated malignancies
• Acute opportunistic infections (OIs)
• Lower CD4 counts (e.g., <200 cells/mm3)
• HIV - associated Nephropathy (HIVAN)
• HIV/Hepatitis B virus co-infection
• HIV/Hepatitis C virus co-infection

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9
Q

What do you look for when monitoring efficacy of ARV’s?

A
  • Weight gain
  • Decrease or disappearance of symptoms
  • Decrease in frequency and/or severity of OIs
  • Increase in CD4+ count of an average of 100 cells per year
  • Sustained suppression of HIV viral loads to undetectable levels
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10
Q

How is HIV trasmitted?

A
  • Sexually
  • Parenterally e.g. transfusion of infected blood, shared IV drug paraphernalia, needle stick injury with infected blood
  • Vertically i.e. mother-to-child transmission (MTCT), which can occur during pregnancy, delivery or breastfeeding
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11
Q

What are the two main types of HIV and how do they cause disease

A

HIV - 1
HIV - 2
Either one can infect a host or both can infect a host.

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12
Q

How many groups of HIV 1 exist and what do they represent?

A

Four groups of HIV-1 exist and represent three separate transmission events from chimpanzees (M, N, and O), and one from gorillas (P)

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13
Q

HIV 1 Subgroups, Clades and Distribution

A

Group M is the cause of the global HIV pandemic; consists of nine clades: A–D, F–H, J, and K
Group N, O, and P are restricted to west Africa

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14
Q

HIV 1 Clade C and B areas

A

Clade C predominates in Africa and India
Clade B predominates in western Europe, the Americas, and Australia

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15
Q

Why is there marked diversity in HIV 1?

A

The marked genetic diversity of HIV-1 is a consequence of the error prone function of reverse transcriptase which results in a high mutation rate

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16
Q

What are the implications for the global distribution of the clades

A

The global distribution of the various clades has implications for vaccines development

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17
Q

Differences between HIV 2 and HIV 1

A

*HIV-2 is largely confined to West Africa and causes a similar illness to HIV-1
* Immunodeficiency progresses more slowly in HIV-2 so it has a longer asymptomatic phase than HIV-1
* HIV-2 is less infectious and less transmissible than HIV-1, with a 5-fold lower rate of sexual transmission and 20- to 30-fold lower rate of vertical transmission
* Persons infected with HIV-2 tend to have a lower viral load than those with HIV-1; the high viral load in HIV-1 infection is associated with more rapid progression to AIDS

18
Q

How is HIV 2 transmitted?

A
  • Perinatal transmission rates of HIV-2 is low with or without intervention (0% to 4%)
  • The commonest mode of HIV-2 transmission is sexually
  • HIV-2 can also be transmitted through breastfeeding
19
Q

Does HIV - 2 protect against HIV -1 and dual infection?

A

HIV-2 infection does not protect against HIV-1 and dual infection, which carries the same prognosis as HIV-1 mono-infection can occur

20
Q

Why is it that most of the research, vaccine and drug development has been focused on HIV-1

A

Because HIV-2 is rare in the developed world, most of the research, vaccine and drug development has been focused on HIV-1

21
Q

Describe the structure of HIV

A
  • An RNA retrovirus- subfamily Lentivirus

Contains:
* 2 copies of RNA
* 3 Enzymes:
Reverse Transcriptase
Integrase
Protease
* Two major envelope proteins:
gp120
gp41

22
Q

What are the steps in the life cycle of HIV in a host cell?

A

Attachment
Co-receptor binding
Fusion
Uncoating
Reverse transcription
Integration
Transcription
Translation
Assembly
Budding
Maturation

23
Q

Which cells are infected by HIV?

A

CD4+ Helper T lymphocytes - Mainly.
* Other cells expressing CD4+ receptors are also infected i.e. monocytes, macrophages and dendritic cells

24
Q

Where does CD4+ independent infection occur?

A

CD4+ independent HIV infection of cells occurs notably in astrocytes (causing HIV-associated neurocognitive disorder) and renal epithelial cells (causing HIV nephropathy)

25
Q

What protein facilitates binding to the CD4 receptors

A

HIV viral-envelope protein-gp120

26
Q

What does Membrane fusion and entry into the host cell require?

A

Membrane fusion and entry into the host cell requires further interaction betweenchemokine co-receptors CXCR4 & CCR5 present on the host cell membrane andgp41

27
Q

Describe the life cycle of HIV from the production of pro-viral DNA to the budding of new viral proteins

A
  • Viral reverse transcriptase catalyzes the conversion of viral RNA into DNA
  • Pro-viral DNA enters the nucleus and becomes integrated into chromosomal DNA of host cell (catalyzed by integrase)
  • Expression of viral genes leads to production of viral RNA and proteins
  • Protease enzyme cleaves proteins into functional mature products
  • Viral proteins and viral RNA are assembled at the cell surface into new viral particles which leave the host through budding
28
Q

Factors contributing to the risk of acquisition of HIV infection

A

The nature of the exposure (the route & size of the inoculum)
The virulence of the virus
The nature of the host susceptibility to infection

29
Q

Compare the risk of acquiring HIV infection from a blood transfusion and needlestick injury

A

Transfusion of HIV-infected blood carries a 95% risk of transmission compared to a 1:300 risk of acquiring HIV from a needle-stick with infected blood

30
Q

Transmucosal infection risks

A

Transmucosal infection risks vary according to the site of exposure with risks of transmission through rectal exposure > vaginal exposure > oral mucosa

31
Q

What other factors increase the risk of HIV transmission

A

The presence of ulcerative STDs, trauma, menstruation and lack of male circumcision increases the risk of transmission

32
Q

When is Mother to Child Transmission of HIV higher

A

MTCT of HIV is higher in women with high plasma HIV RNA

33
Q

Waht foru mechanisms explain the syndromes caused by HIV infection?

A

Immunodeficiency
Chronic inflammation and immune activation
Autoimmunity
Allergic and hypersensitivity reactions

34
Q

Cause of Immunodeficiency in HIV

A

Immunodeficiency is a direct result of the effects of HIV upon immune cells causing a spectrum of OIs and neoplasms

35
Q

What causes the inflammation and immune activation

A

The chronic viral infection causes a generalized state of inflammation and immune activation resulting in a spectrum of diseases

36
Q

What are the most common clinically apparent manifestations of HIV?

A

Autoimmunity, allergic and hypersensitivity reactions may be the only clinically apparent manifestation or may coexist with obvious manifestations of immunodeficiency

37
Q

Why does autoimmunity occur in HIV?

A

Autoimmunity can occur as a result of disordered cellular immune function or B lymphocyte dysfunction e.g. include Lymphocytic interstitial pneumonitis, Immunologic thrombocytopenia

38
Q

Allergic and hypersensitivity reactions in HIV patients

A
  • HIV infected individuals tend to have higher rates of allergic reactions to unknown allergens e.g. eosinophilic pustular folliculitis.
  • HIV infected individuals have increased rates of hypersensitivity reactions to medications
39
Q

What are the three stages of HIV infection. How does progress through these stages vary from person to person?

A

Acute HIV infection - High viral load, Low CD4 count. Lasts weeks to months
Chronic HIV infection - Viral load drops and rises slowly. CD4 count rises a bit and progressively declines.
AIDS

  • The time it takes for each individual to go through these stages varies

*For the majority of people however, the progression of HIV disease is fairly slow, taking several years from infection to development of AIDS

40
Q

What is Acute HIV infection?

A

Is the period of time between the initial HIV infection and seroconversion usually 6 to 12 weeks, rarely up to 6 months