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I & I Part II > HIV Pathogenesis and Immunity > Flashcards

HIV Pathogenesis and Immunity Flashcards

1
Q

CXCR4 predominantly expressed on [] cells.

A

CXCR4 predominantly expressed on naïve CD4 T cells.

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2
Q

CCR5 predominantly expressed on [] cells.

A

CCR5 predominantly expressed on memory CD4 T cells, macrophages, monocytes, Langerhans cells of skin, perivascular macrophages, microglial cells.

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3
Q

The first cells to be infected with HIV are [].

A

The first cells to be infected with HIV are macrophages, Langerhans cells, mucosal T-cells – CD4+/CCR5+ cells.

  • Infects efficiently and kills specifically the CD4+ T4 lymphocytes, initially mucosal T cells, characterized by loss of CD4+ T4 lymphocytes
  • Can establish persistent infection characterized by the presence of replicating virus with little immunological abnormalities – clinical latency
  • Antiretroviral therapy creates viral latency in many infected patients
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4
Q

[] acts on the LTR sequences known as TAR to increase the rate of viral transcription and may stabilize the RNAs.

A

Tat acts on the LTR sequences known as TAR to increase the rate of viral transcription and may stabilize the RNAs.

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5
Q

[] transports structural proteins mRNA from the nucleus to cytoplasm.

A

Rev transports structural proteins mRNA from the nucleus to cytoplasm.

  • Rev binds to rev responsive element (RRE), located in the env gene.
  • Rev may also be involved in splicing and stability of mRNAs
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6
Q

Nef

A

down regulates CD4+ expression, required for viral pathogenesis

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7
Q

Vif

A

increase virus infectivity

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8
Q

Vpr

A

Prevents cell proliferation, arrest cells in G2/M phase, upregulates virus expression

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9
Q

Vpu

A

Virus release and/or assembly

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10
Q

Vpx

A

in HIV 2 - Virus release and/or assembly

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11
Q

Genetic Variation in HIV

A
  • HIV-1 possesses the most error-prone reverse transcriptase among all retroviruses
  • Several variants or genotypes exist within an infected individual and clades and subtypes in infected population
  • Clade M (major), O (outlier), N (new)
  • M clade has A-H subtypes, B subtypes in the U.S.
  • The variability is mainly in envelope region because of the immunologic pressure but also observed in other regions of the genome
  • Results in change of cell tropism, replication level, virulence, immune escape
  • Genetic variation causing problems in vaccine development
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12
Q

Pathogenesis of HIV

A
  1. Transmission of HIV (common route: sexual route)
  2. Acute phase of intense viral replication and dissemination to lymphoid tissues (acute-retroviral syndrome; flu or mono-like illness
  3. Activation of innate and adaptive immune response, unable to contain highly replicating/ mutating virus
  4. Persistent asymptomatic phase (clinical latency) of continued viral replication and immune activation
  5. Advanced phase of marked depletion of CD4 T lymphocytes (immune deficiency) leading to development of AIDS (opportunistic infections)
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13
Q
A
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14
Q

HIV Immune Response

A
  • Early control by innate immunity and later adaptive to cause virus set point
  • APCs present antigen to T cells to generate CD8+CTLs that kill HIV infected cells and control viremia, CTL escape mutants develop due mutation
  • B cells respond to HIV antigens, collaborates with CD4 T cells to make neutralizing antibodies that also controls viremia, viral escape variants emerge
  • Early in infection memory CD4+ T cells (mucosal) are depleted, but late in infection all CD4+ T cells are depleted causing immunodeficiency
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15
Q

HIV Immune Activation

A

Production of proinflammatory cytokines, TNF-a, IL-1, IL-6, IL-12, chemokines, IFN-a and LPS

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16
Q

Neutralizng Antibodies

A

HIV-1 gp120 and gp41 are the major target for humoral antibody response, the principal neutralizing domain (PND) is the variable 3 (V3) region, antibodies against most of HIV-1 proteins can be found in infected patients.

17
Q

CD4+ T Cells Response

A

viral peptides presented by DC on MHC II to CD4 T cells, release of antiviral cytokines (INF-γ, TNF-α), help for antiviral antibody production

18
Q

CD8+ T Cells Response

A

viral peptides presented by DC on MHC I to CD8 T cells, killing of virus infected cells, release of antiviral substances

19
Q

Enhancing Antibodies

A

enhances HIV infection

20
Q

Latency

A
  • Clinical latency observed in HIV-1 infection that is long asymptomatic period following HIV infection
  • Several factors can terminate clinical latency such as mutations, altered cell tropism, activation of infected T cells by mitogens and DNA viruses
  • Patients treated with anti-retroviral therapy (ART) have significant decrease in viral load and increase in CD4 T cells count.
  • Therefore, HIV becomes latent (low level to no viral replication) in resting T-lymphocytes, central memory T-lymphocytes, CD34 hematopoietic progenitor stem cells, and monocytes/ macrophages.
21
Q

Immunodeficiency

A

CD4+ T cells depletion leads to generalized failure of cell mediated immunity resulting in opportunistic infection and malignancy

22
Q

Depletion of HIV-1 infected CD4+ T cells

A
  • No damage to the cells with very low or no virus
  • Active virus production leads to cell death
  • Humoral or cell mediated response may also lead to destruction of infected cell
  • CD4+ cells surface expressing gp120 and gp41 can be killed by antibody-plus-complement lysis
  • Cells expressing viral peptides with MHC I are killed by CTL response
  • Lymph nodes contain 10 to 100 times more virus than circulating CD4+ T cells
23
Q

Destruction of CD4+ T Cells

A
  • In HIV infected individuals: normal to 50/ul
  • In HIV infected patients, CD4+/CDB+ ratio is: 1.0 to 0.2 (normal CD4+/CD8+ ratio is 2.0)
  • Opportunistic infections are based on CD4 counts
  • Regeneration capacity of CD4 and CD8 cells is diminished in infected patients
24
Q

Depletion of uninfected CD4+ T cells

A
  • Syncytia formation and destruction by soluble gp120
  • Interference with T-cell maturation
  • Inappropriate programmed cell death
25
Q

HIV Reservoirs

A
  • GALT and Lymph Nodes
  • Resting CD4+ T lymphocytes remain silently infected with HIV provirus
  • The phenotype of these CD4+ T cells includes central memory CD4+ T cells (TCM), transitional memory CD4+ T cells (TTM) and effector memory CD4+ T cells (TEM)
26
Q

Failure of the Immune System to Eliminate HIV Infection

A
  • Cell-to-cell spread avoids virus recognition by antibodies
  • High rate of mutation results in antigenic variation
  • Virus escapes from antibody and CTL recognition
  • Immune system unable to keep the pace with rapidly mutating virus
  • Suppression of MHC I and II, interference with cytokine
  • Establishing persistent infection
  • Integration of viral genome into host chromosome
  • Impaired T and B cell function, finally development of AIDS with opportunistic infections

I & I Part II (25 decks)

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