INFECTIOUS DISEASE Flashcards

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1
Q
A
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2
Q

Coxsackie A

A

Enterovirus, Icosahedral, +ssRNA

Herpangina
Hand, foot, and mouth disease
Pericarditis , myocarditis
Aseptic meningitis

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3
Q

Coxsackie B

A

Enterovirus, Icosahedral, +ssRNA

Myocarditis
Dilated cardiomyopathy
Bornholm disease
Pericarditis
Aseptic meningitis

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4
Q

What are the HIV key enzymes?

A
  • Reverse transcriptase
  • Aspartate protease
  • Integrase
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5
Q

How is the HIV structure?

A
  • Phospholipid membrane containing Env proteins
  • On the cap of the Env : Glycoproteins (gp 120, gp41)
  • Cone-shaped capsid contaning multiple p24 proteins
  • Carries 2 copies of RNA
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6
Q

What are de glycoproteins from the HIV membrane and what are their functions?

A

gp 120: Attachment to T-cells
gp41: Fusion and entry into T-cells

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7
Q

What is the key feature about gp120 glycoprotein from HIV membrane to know?

A

Antigenic variation - mutates rapidly difficulting antibody neutralization

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8
Q

What are the main genes that encodes major parts of the HIV virus?

A

Gag: nucleocapsid
Pol: Polymerase
Env: envelope proteins

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9
Q

What Env gene encodes?

A

Envelope proteins
gp160 that is cleaved in gp120 and gp41

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10
Q

What are the two regulatory genes of the HIV and what their funtions?

A

Tat: Activates transcription of genes
Rev: Transports mRNA from nucleus to cytoplasm

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11
Q

What are the auxiliary genes of the HIV?

A

Nef
Viv
Vpr
Vpu
Vpx

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12
Q

What is the function of the Nef gene on HIV?

A

Decrease CD4 proteins and MHC I on T-cell surface

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13
Q

What are the two receptors on immune cells that HIV binds to get entry into the cell?

A

CCR5 and CXCR4

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14
Q

In wich cells the HIV replicates more efficiently when is CCR5-tropic?

A

Monocytes/ Macrophages
Dendritic cells

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15
Q

In wich cells the HIV replicates more efficiently when is CXCR4-tropic?

A

T-cells

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16
Q

What are the differences between HIV-1 and HIV-2?

A

HIV-2 is a cause of infection in West Africa and don’t respond to NNRTIs

17
Q

For what the CD 4 T-cell count is used?

A

Follow treatment response
Initiate prophylaxis

17
Q

What are the markers of HIV infection used to monitor effectiveness of the drug therapy?

A

CD4 T-cells count
HIV RNA quantification

18
Q

What are the parameters used to diagnose AIDS?

A

CD 4 < 200cells/mm3 or AIDS-definig infections

19
Q

What is the most important cells during clinical latency of HIV infection?

A

CD8 T-cells

20
Q

How HIV causes dementia?

A

Infections of macrophages that entry in the CNS and also infect microglia cells

21
Q

How is the HIV test for diagnoses?

A

Acute : HIV RNA testing (viral load)
Chronic : Test for p24 and HIV antibodies

22
Q

What is the test for Acute HIV?

A

HIV RNA testing (viral load)

23
Q

How perinatal HIV is diagnostic?

A

HIV PCR test

24
Q

When the prophylaxis are given for HIV patients?

A
  • CD4< 200 :
  • TMP-SMX : Pneumocystis pneumonia
  • CD4 < 100 :
  • TMP-SMX: Pneumocystis and Toxoplasmosis
  • Itraconazole: Histoplasmosis (endemic area)
  • CD4<50 :
  • Azithromicin: Mycobacterium avium complex
25
Q

What is IRIS in HIV?

A

Immune Reconstitution Inflamatory Syndrome: Flare of infections symptoms with HIV treatment

26
Q

A 34-year-old man with newly diagnosed HIV presents with a CD4 count of 38 cells/mm³ and a viral load of 600,000 copies/mL. He is started on antiretroviral therapy with tenofovir, emtricitabine, and dolutegravir. Four weeks later, he returns with new complaints of fevers, worsening cough, and night sweats. Physical examination reveals lymphadenopathy and hepatosplenomegaly. A chest X-ray shows new mediastinal lymphadenopathy. Blood cultures and sputum cultures are negative for bacteria, fungi, and viral pathogens.

Which of the following mechanisms is the most likely cause of his symptoms?

A) Drug hypersensitivity reaction to dolutegravir
B) Reactivation of latent cytomegalovirus infection
C) Immune response to previously undiagnosed infection due to immune reconstitution inflammatory syndrome (IRIS)
D) Progressive disseminated mycobacterial infection due to low CD4 count
E) Tenofovir-induced Fanconi syndrome

A
27
Q

28-year-old man presents to the clinic for HIV testing. He reports recent weight loss, fatigue, and night sweats. Initial testing confirms HIV infection. Molecular analysis shows that the predominant viral strain in his body binds preferentially to the CCR5 co-receptor.

Which of the following statements best describes the characteristics of the CCR5-tropic strain of HIV in this patient?

A) This strain primarily infects CD8+ T cells
B) CCR5-tropic strains are typically found in the early stages of infection and primarily infect macrophages and dendritic cells
C) The presence of CCR5-tropic strains is an indication of long-standing HIV infection
D) CCR5-tropic HIV does not require binding to CD4 for cellular entry
E) CXCR4-tropic strains are more likely to lead to rapid progression to AIDS

A
28
Q

A 32-year-old woman with HIV is started on antiretroviral therapy, including tenofovir, emtricitabine, and ritonavir-boosted darunavir.

Which of the following statements best explains how ritonavir improves the efficacy of darunavir in this patient’s treatment regimen?

A) Ritonavir acts as an entry inhibitor, preventing viral attachment to CD4 cells
B) Ritonavir boosts darunavir’s efficacy by inhibiting the HIV integrase enzyme
C) Ritonavir enhances the plasma concentration of darunavir by inhibiting the cytochrome P450 enzyme system
D) Ritonavir acts as a nucleotide analog, causing chain termination in viral replication
E) Ritonavir induces mutation in the viral genome, leading to decreased viral replication

A
29
Q

A 29-year-old man with HIV presents with fever, fatigue, sore throat, and generalized lymphadenopathy. He reports that these symptoms began three weeks after unprotected sexual contact with a new partner. His CD4 count is 700 cells/mm³, and his viral load is markedly elevated.

Which of the following best describes the likely phase of HIV infection in this patient?

A) Acute HIV infection with high viremia and non-specific viral syndrome
B) Clinical latency with steady decline in CD4 count
C) Early-stage AIDS with increased risk of opportunistic infections
D) Immune reconstitution inflammatory syndrome due to ART initiation
E) Advanced HIV infection with decreased viral replication

A
30
Q

A researcher is studying the role of the HIV nef gene in infected T cells. A viral strain with a deletion in the nef gene is found to replicate less effectively in vitro.

Which of the following best explains the function of the nef gene in HIV infection?

A) Promotes entry of HIV by enhancing binding of GP120 to the CD4 receptor
B) Enhances transcription of viral RNA by activating reverse transcriptase
C) Reduces expression of CD4 and MHC-I on the host cell surface, helping HIV evade the immune response
D) Facilitates viral genome integration by activating integrase
E) Enhances GP41-mediated fusion of the viral envelope with the host cell membrane

A
31
Q

A 40-year-old man with HIV has been on antiretroviral therapy for several years. His regimen initially included zidovudine, lamivudine, and efavirenz. However, recent viral load testing shows an increase in HIV RNA levels, suggesting drug resistance. A genotype analysis reveals a K103N mutation in the reverse transcriptase enzyme.

Which of the following best explains this patient’s drug resistance?

A) Resistance to zidovudine due to alteration in thymidine kinase activity
B) Resistance to lamivudine due to reduced incorporation into viral DNA
C) Resistance to efavirenz due to a mutation in the non-nucleoside reverse transcriptase inhibitor (NNRTI) binding site
D) Resistance to protease inhibitors due to mutations in the pol gene
E) Resistance to integrase inhibitors due to enhanced integrase binding affinity

A
32
Q

A 26-year-old man presents to the emergency department with a two-week history of fever, myalgia, and sore throat. He reports recent unprotected sex. His rapid HIV antibody test is negative, but his symptoms and exposure history raise suspicion for acute HIV infection.

Which of the following tests would be most appropriate to confirm the diagnosis of acute HIV in this patient?

A) Western blot for HIV-1 antibodies
B) Repeat HIV antibody test in 6 weeks
C) HIV p24 antigen test
D) Plasma HIV RNA (viral load) test
E) CD4/CD8 ratio assessment

A
33
Q

A 45-year-old man is diagnosed with HIV. Genetic testing of the virus reveals it predominantly uses the CXCR4 co-receptor for cell entry. He is started on a standard antiretroviral regimen, including a CCR5 antagonist.

Which of the following best explains why the use of a CCR5 antagonist is ineffective in this patient?

A) CXCR4-tropic HIV does not require CD4 for entry into host cells
B) CCR5 antagonists only inhibit binding to monocytes and macrophages
C) CXCR4-tropic HIV strains do not use the CCR5 co-receptor, so blocking CCR5 has no effect
D) CXCR4-tropic strains are resistant to all forms of antiretroviral therapy
E) CCR5 antagonists only prevent viral replication in the CNS

A
34
Q

A 33-year-old woman with advanced HIV and a CD4 count of 80 cells/mm³ is brought to the emergency department with a one-week history of fever, headache, and altered mental status. Physical examination reveals nuchal rigidity. Lumbar puncture is performed, and cerebrospinal fluid (CSF) analysis reveals elevated opening pressure, low glucose, and positive India ink staining.

Which of the following is the most likely diagnosis?

A) Cytomegalovirus (CMV) encephalitis
B) Cryptococcal meningitis
C) Toxoplasma encephalitis
D) Progressive multifocal leukoencephalopathy (PML)
E) Herpes simplex virus (HSV) encephalitis

A
35
Q

What regulatory gene is needed for progression from HIV infection to AIDS?

A

NEF

36
Q
A