1. viral transmission
2. helper T cell count falls and viral load rise w/ active viral replication in lymphoid tissue
3. seroconversion 3 weeks post transmission
4. six months after transmission, individual reaches setpoint on viral load (higher set pt = more rapid disease progression)
5. asymptomatic chronic phase of infection (clinically, but not virologically latent)
   • can be with or w/o lymphadenopathy
   • usually see follicular hyperplasia
6. average CD4 cells decline 50 per year (correlates with viremia)
7. w/o antiretrovirals, should develop AIDS

• dramatic fall in viremia
• mechanism- rise in cytotoxic lymphocytes and neutralizing antibodies

• fever
• adenopathy
• pharyngitis
• rash
• mucocutaneous ulceration of mouth, esophagus, or genitals
• myalgias, arthralgias
• diarrhea
• headache
• nausea/vomit
• hepatosplenomegaly
• thrush
• meningoencephalit6is
• peripheral neuropathy

• thrush
• oral hairy leukoplakia (EBV)
• peripheral neuropathy
• cervical dysplasia
• fever
• weight loss
• herpes zoster
• ITP

1. clinically latent phase- explosive follicular hyperplasia
2. in course of HIV
   1. mixed follicular hyperplasia and involution w/ follicular lysis
   2. follicular involution
   3. lymphocytic depletion aka atrophic

Parallel stage of disease and degree of immunodeficiency.

1. viral envelope spikes (gp12) use the chemokine co-R of:
   • macrophages: CCR-5
   • CD4 cells: CXCR-4

Early in disease, there is a predominance of macrophage tropic virotypes, and when conversion to lymphotropic strains takes place, patient has accelerated infection and finally AIDS.

• MIP1 alpha
• MIP1 beta
• RANTES

Chemokine binds to R on T cells and macrophages resulting in blockage of co-R of HIV entry into that cell

memory CD4 T cells

• CD4 T cell count below 200
• qualifying opportunistic infection
• qualifying malignancy
  • Kaposi's sarcoma
  • lymphoma
  • carcinoma
  • cervical carcinoma
• HIV encephalopathy
• HIV wasting syndrome

• for life OR until CD4 count rises above 200 cells

• viral DNA integrates into host nuclear DNA as a provirus
  • more latently infected than productively infected cells in host
• has high error rate of replication "antigenic variants"
  • reason for common development of drug resistance

• during initial weeks of infection, HIV will replicate in activated CD4 T cells
• as CD4 cells are activated, this increases CD4 susceptibility to HIV infection
• after that, the host is left without specific CD4 cells to provide help to cytotoxic T cells and B cells

only infection of man to go from acute to chronic stage with persistent replication of virus and both humoral and cellular immunity

• few if any remnants of follicles
• hypocellular sea of macrophages and plasma cells
• cells are dispersed in non-sclerosing background

• B cell types
• Burkitt's and Burkitt's like
• diffuse large cell lymphoblastic cyte
• immunoblastic variant of diffuse large cell lymphoma
• Hodgkin's disease
• most are extranodal
  • CNS lymphomas (associated with EBV)
  • GI

• lesion of lymphatic endothelial cells
  • so, it will not appear in CNS, which lack lymphatics
• common site- lymph nodes
• prognosis- totally reversible when immunocompetence is restored in HIV/AIDS and transplatnt patients

• spindle shaped endothelial cells
• complicated slit like vascular channels filled with RBC's
• lesions are multifocal proliferations of HHV-8 infected endothelial cells
  • probably hyperplastic, NOT neoplastic/ metastatic process
  • BUT, proliferating cells could eventually become autonomous and truly neoplastic and metastasize