ORAL REVALIDA 3 Flashcards

1
Q

What family does HIV belong to?

A

Retroviridae

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2
Q

What disease does HIV cause?

A

Acquired Immunodeficiency Syndrome (AIDS)

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3
Q

What are the two main HIV serogroups?

A

• HIV-1 (predominant, found worldwide).
• HIV-2 (mainly in West Africa).

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4
Q

What are the three subtypes of HIV-1?

A

M, N, and O, with M being the major subtype.

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5
Q

What cells does HIV bind to?

A

CD4+ T helper cells, monocytes, and macrophages

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6
Q

What role do co-receptors play in HIV infection?

A

They assist viral binding to host cells.

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7
Q

How does HIV enter the host cell?

A

It penetrates the plasma membrane, releasing its RNA.

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8
Q

What enzyme transcribes HIV RNA into DNA?

A

Reverse transcriptase.

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9
Q

How is viral DNA integrated into the host genome?

A

Using the viral enzyme integrase.

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10
Q

How does HIV replicate inside the host cell?

A
  1. Viral DNA is transcribed into mRNA.
    1. mRNA is translated into viral proteins.
    2. New viruses bud from the host cell.
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11
Q

What is the effect of HIV replication on the immune system?

A

It kills infected T helper cells, reducing their number over time.

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12
Q

When do HIV antibodies first appear?

A

Around 12 weeks after infection.

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13
Q

What tests detect these initial antibodies?

A

ELISA and Western blot.

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14
Q

What are neutralizing antibodies, and when do they appear

A

• Antibodies that interfere with viral infection.
• Appear 1 year after infection.

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15
Q

Why is the immune system unable to eliminate HIV?

A

HIV undergoes antigenic variation, allowing it to evade the immune response.

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16
Q

What happens to CD4+ T helper cells as HIV progresses?

A

They decrease, leading to worsening immune deficiency

17
Q

Why is the loss of T helper cells critical?

A

They are essential for both humoral and cellular immunity.

18
Q

How does HIV affect the CD4:CD8 ratio?

A

It decreases from the normal 2:1 ratio.

19
Q

How does HIV affect other immune cells?

A

• Decreased natural killer (NK) cell activity.
• Defective monocyte and macrophage chemotaxis.
• Increased release of interleukin-1 and cachectin by monocytes.

20
Q

How is HIV-1 transmitted?

A

Through:
• Unprotected sex
• Contaminated blood/products
• Contaminated needles
• Perinatal transmission

21
Q

AIDS in the us

A

AIDSVis the leading cause of death in people aged 20–35 in the US

22
Q

What are the symptoms of acute HIV infection?

A

Usually asymptomatic, but may resemble infectious mononucleosis (IM).

23
Q

What is clinical latency in HIV?

A

A stage where the virus replicates in lymphoid tissue without major symptoms.

24
Q

What is AIDS-related complex (ARC)?

A

A stage where opportunistic infections (e.g., Candida, herpes simplex, CMV) begin as T cells decline

25
Q

What defines full-blown AIDS?

A

Severe CD4+ T cell depletion and life-threatening opportunistic infections/cancers, including:
• Esophageal candidiasis
• Cryptococcosis
• Cytomegalovirus (CMV) & herpes simplex infections
• Pneumocystis jiroveci pneumonia (PJP)
• Kaposi’s sarcoma

26
Q

How is the severity of HIV/AIDS staged?

A

By CD4+ T cell counts and the presence of opportunistic infections.

27
Q

What is the primary screening test for HIV?

A

ELISA, which detects HIV antibodies and antigens.

28
Q

How is an HIV diagnosis confirmed?

A

By a Western blot or immunofluorescence assay.

29
Q

What criteria make a Western blot positive?

A

The presence of at least two of the following bands:
• p24
• gp41
• gp120/gp160

30
Q

What molecular tests detect HIV?

A

• Genetic probes detect replicating viruses.
• RT-PCR (Reverse Transcriptase PCR) detects HIV-1 and HIV-2 nucleic acids.
• Indirect immunofluorescence assay detects HIV antigen in infected cells.

31
Q

What is the main HIV treatment?

A

Antiretroviral therapy (ART), including Zidovudine (Retrovir).

32
Q

How does Zidovudine help?

A

• Increases survival time
• Decreases mortality

33
Q

What are the roles of GP-120 and GP-41 inhibitors in HIV treatment?

A

• GP-120 inhibitors: Prevent virus attachment and entry into cells.
• GP-41 inhibitors: Block virus fusion with immune cells.

34
Q

Does ART cure HIV?

A

No, it suppresses the virus but does not eliminate it. The virus can still hide in tissues (latency phase) and reactivate if treatment stops.

35
Q

What are the six classes of antiretroviral drugs?

A
  1. Attachment Inhibitors
  2. Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
  3. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
  4. Protease Inhibitors
  5. Integrase Inhibitors
  6. Pharmacokinetic Enhancers (Boosters)
36
Q

What are the key HIV prevention strategies?

A

• Modifying sexual behavior (e.g., using condoms, reducing partners)
• Protecting blood supply (e.g., donor screening, heating plasma at 68°C for 24 hours)
• Encouraging self-referral among high-risk groups

37
Q

Why is an HIV vaccine difficult to develop?

A

• Rapid mutations create multiple strains.
• HIV hides in immune cells, making it hard to target.
• The virus infects the very immune cells a vaccine would stimulate.