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I&D > week 3 day1: HIV, Herpes > Flashcards

week 3 day1: HIV, Herpes Flashcards

1
Q

What part of the virus Allows attachment to host cells?

A

Membrane glycoP (peplomer)

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2
Q

What part of the virus encapsulates the genetic material? what is it made of?

A

Capsid, protein coat

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3
Q

Part of the virus that surves as an extra protective layer?

A

lipid envelope

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4
Q

4 things determining viral pathogenesis?

A
  • Interaction with specific host cells
  • Interaction with the immune system
    • Immune escape
    • Immune modulation or immune evasion
    • Avoiding immune surveillance
  • Host immune response causing pathology
  • Cellular transformation - cancer
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5
Q

What cellular product is released once our PRRs sense viral PAMPs? What are its functions?

A

Type 1 IFNs- - Direct anti-viral actions; Limits viral spread between cells

  1. increases cytotoxicity of NK and CD8 T cells
  2. activate signals to kill infected cells
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6
Q

What are the role of T cells and antibodies during a viral invasion?

A

Memory T cells prevent reactivation of latent virus

Antibodies neutralize virus on re-exposure

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7
Q

What does HIV mainly targets?

A

decreases CD4 T helper lymphocytes

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8
Q

What are the two glucoproteins of HIV and what are their functions?

A

gp120 - docking P, attaches to host receptor CD4, and CCR5/CXR4 coreceptor

and gp41 - fuses viral envelope to CW of the host (transmembrane glycoprotein)

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9
Q

What are the three structural genes of HIV and how do they contribute to HIV infection?

A

gag - encodes internal P

pol -encodes reverse transcriptase, viral RNA→DNA

env. -gp120(binds CT4 on T cells) and gp41 (mediates fusion of viris and cellular membrane of a host)

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10
Q

What do the genes responsible for regulating encode?

A

replication and uncoating of HIV genome and also production of virus particles

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11
Q

Steps of the HIV cycle?

A
  1. HIV attaches with GP120 to hosts CD4 and CCR5
  2. viral GP4 fuses virus with hosts CM
  3. Reverse transcription RNA→DNA
  4. Integrase helps viral DNA to integrate into hosts
  5. after transcription and translation protease cleaves viral polyP from host genome and mature virus exits
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12
Q

What are the three tests for HIV? Benefits and negatives of them?

A
  1. Antibody to envelope glycoP - takes long time for antibodies to be detectable (3-12 weeks!)
  2. Antigen tests - like for gag genes. Takes less time (2-6 weeks), Combo of Ag and Ab tests are rapid and now are more common
  3. Nucleic acid tests (PCR) - 1-4 weeks. fast but expensive, only for high risk exposure
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13
Q

What are the three stages of HIV infections and what are the manifestations?

A
  1. weeks 2-4 Acute HIV syndrome - wide dissemination of virus and huge dip in CD4 cells. Very infectious. Many develop Flu like symptoms
  2. Clinical latency - can be asymptomatic and HIV is hiding in lymph nodes. No symptoms or only mild ones. Still able to transmit to others
  3. AIDS - CD4 lymphocytes die out and a person is susceptible to opportunistic (most common - fungal) infections and cancer.
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14
Q

What are the three most common HIV co-infections?

A

HepB (10% of HIV patients)

Hep C (25%)

TB

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15
Q

What are the 8 families of Herpesviridae?

A
  1. HSV-1 Herpes simplex virus 1 - herpes labialis (cold Sores)
  2. HSV-2 Herpes simplex virus 2 - genital herpes
  3. VZV - Varicella Zoster Virus - Chicken pox, Shingles
  4. EBV - Epstein-Barr Virus - infectious mononucleosis, Burkitts lymphoma
  5. CMV - Cytomegalovirus - Congenital CMV infection
  6. HHV-6 Human herpesvirus -6-Roseola
  7. HHV-7 Human herpesvirus-7 -roseola
  8. KSHV - Kaposi’s sarcoma - associated Herpesvirus - Kaposi’s sarcoma
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16
Q

What are the group are the families HSV-1, HSV-2 and VZV associated with and what are the developmental features of that group?

A

Alpha Group

  • short Reproductive cycle
  • Efficient destruction of infected cells
  • Rapid spread in culture
  • latency in sensory ganglia
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17
Q

What are Group are the families CMV (5), HHV-6, HHV-7 associated with and what are the developmental features of that group?

A

Beta Group

Long reproductive cycle

Enlargement of infected cells

Slow cell-to-cell spread in culture

Multiple non-ganglionic latency sites

18
Q

What are group are the families EBV, KSHV (HHV-8) viruses associated with in terms of the disease progression and developmental features?

A

Gamma Group

Replication in lymphoblastoid cells

Latency in lymphoid tissue (EBV),

monocytes & B lymphocytes (HHV-8)

19
Q

Disease manifestation of HSV1?

A

Oral Herpes

•Gingivostomatitis;

herpes labialis (cold sores)

  • Eye infections
  • Cutaneous infections; whitlow
  • Encephalitis

Can infect genitals

20
Q

Disease manifestation/symptoms of HSV2?

A
  • Genital herpes; herpes genitalis
  • Neonatal infections

Can infect orally

21
Q

What are some immunocompromised states that makes people more susceptible to HSV?

A
  • Newborn infants
  • Congenital immunodeficiencies (NK & TLR deficiencies, T cell > B cell)
  • Acquired Immunodeficiency Syndrome
  • Immunosuppressive therapy
  • Transplant recipients (BMT)
  • Compromised skin barriers (eczema, burns)
22
Q

What is Primary Gingivostomatitis? What virus causes it? Manifestation? Incubation period? treatment?

A
  • HSV-1 in oral mucosa of children
  • Infection ranges from mild or inapparent to severe, with high fever and toxicity. Painful lesions occur on the buccal mucosa, tongue, gingiva, and pharynx
  • Lesions ulcerate and resolve in 5-12 days
  • Incubation: 2-10 days
  • no tx, self resolve
23
Q

What is herpes labialis? What virus causes it? Manifestation? What causes the recurrence? Tx?

A

Normal Cold Sores- Lesions (on the vermilion border of the lip) caused by HSV-1

  • Recurrence often produces prodrome of itching and tingling followed by 1-2 cm vesicular lesions
  • Called “fever blisters” or “cold sores”
  • Heal spontaneously in 5-7 days, except in immunocompromised
  • Recurrence: stress, illness, severe fatigue, & menstruation triggers

Tx: Acyclovir or Valacyclovir- prevents transmission and reoccurrences

24
Q

What is Herpetic Whitlow? What virus causes it? Manifestation?

A

Recurrent HSV infection of finger and hand, resulting from passage of virus into break in skin caused by HSV-1 60%; HSV-2 40%

Vesicular lesions on finger become pustular, cause severe pain, loss of feeling, & prolonged morbidity

Can happen at any skin cut

Often misdiagnosed as staph and mistreated by antibiotics or incision

25
Q

What is Herpetic Keratoconjunctivitis? What virus causes it? Manifestation? Tx?

A

Ulceration of the cornea from latent virus living in nerve cells of the skin or eye (HSV-1), or direct inoculation from lesions (HSV-1 or 2)

Occasionally deeper ulcers develop & produce stromal keratitis and blindness- dendritic ulcers

Acyclovir - topical

26
Q

What is Herpes Encephalitis? Age? What virus causes it? Tx & prognosis? Can it result from primary infection?

A

Viral encephalitis caused by HSV 2 mostly sometimes 1 (10%)

Bimodal -Ages 10-20 and over 50

80% mortality if untreated,

Also causes Mollaret’s a rare recurring not often fatal meningitis caused by mainly HSV but sometimes other viruses

tx: IV acyclovir

Can be a result of a primary infection HSV-2 (1-3%)!

Diagnosed via CSF test

27
Q

Steps of How varicella Ifection happens?

A

Starts with Resp. tract and conjunctiva in epithelial cells

Local replication in upper airway & regional lymph nodes

Primary viremia & infection of lymphocytes & nerve cells

Replication & secondary viremia Replication & secondary viremia

Infection of skin Infection of skin (day 10-21)

28
Q

Steps of How varicella Infection happens?

A

Starts with Resp. tract and conjunctiva

Local replication in upper airway & regional lymph nodes

Primary viremia & infection of lymphocytes & nerve cells

Replication & secondary viremia Replication & secondary viremia

Infection of skin Infection of skin (day 10-21)

29
Q

What are the Immune privileged sites?

A

Tissues that are in part protected from the immune system

Brain, nerves, eyes, testes, placenta/fetus

30
Q

What are the risk factors for Shingles?

A

HIV patients

T cell dysfunction or absence in older patients

31
Q

What are the symptoms of cytomegalovirus (CMV/HHV-5)? Prevalence? What disease can it cause? How is the virus shedding?

A

In HIV retinitis, Colitis in IBD and transplant patients

50-60% of people in US have it, 30% by age 5 100% in developing countries

Most people are asymptomatic, its easily transmittable

Most people carry it in latent phase without symptoms for life

Can cause mononucleosis (8% of mono cases)

Shedding in saliva and urine

31
Q

What are the symptoms of cytomegalovirus (CMV)? What disease does it cause? How is the virus shedding?

A

Most people are asymptomatic, its easily transmittable

Most people carry it in latent phase without symptoms for life

Can cause mononucleosis (8% of mono cases)

Shedding in saliva and urine

32
Q

replication sites of EBV KSHV (HHV-8)? Where do they stay latent?

A

Replication in lymphoblastoid cells

Latency in lymphoid tissue (EBV) and monocytes & B lymphocytes (HHV-8)

33
Q

Symptoms of EBV? What can EBV cause?

A

most without symptoms

infects epithelial oropharyngeal(can cause sore throat) and then infect B cells

Then T cell activation and A-typical lymphocytes leads to enlargement of lymph nodes,liver and spleen

Its widely spread (90%) - asymptomatically shed
Can cause mononucleosis, EBV-associated malignancies

34
Q

What are the two viruses mainly cause mononucleosis?

A

EBV, CMV and other herpesviruses

Several others can and bacteria,fungal and protozoa can contribute

35
Q

What are some malignancies associated with EBV? What type of genes are expressed?

A

Burkitts Lymphoma, Hodgkin’s lymphoma, nasopharyngeal carcinoma, Oral hairy leukoplakia, CNS lymphoma, post transplant lymphoproliferative disease

No lytic genes only latent

36
Q

Oral Hairy Leukoplakia (OHL)? What are the symptoms?

A

Lingual squamous epithelium, lots of replication and EBV proteins

Not premalignant.

Firm, does not scrape off with blade

37
Q

What are the symptoms of KSHV (HHV-8)? What does it infect?

A

Classic, AIDS-related or secondary to immunosuppressants - can lead to Kaposi’s sarcoma

Infects B cells, macrophages, epithelial cells, endothelial cells, & keratinocytes

38
Q

What are symptoms of Kaposi’s sarcoma? Causative agent?

A

Causative agent - KSHV (HHV-8)

Primary effusion lymphoma
Castleman’s disease (a lympho-proliferative disorder-overgrowth of cells in lymph nodes)

39
Q

What cells does Kaposi sarcoma (HHV-8) infects?

A

B cells

Macrophages

Epithelial cells

Endothelial cells

Keratinocytes

I&D (19 decks)

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