The natural history of AIDS begins with infection by the HIV retrovirus, which is detectable only by laboratory tests, and ends with death. The HIV virus may enter the body by any of several routes involving the transmission of blood or body fluids, for example:

HIV strikes helper T cells bearing the CD4⁺ antigen. Normally a receptor for major histocompatibility complex molecules, the antigen serves as a receptor for the retrovirus and allows it to enter the cell. Viral binding also requires the presence of a coreceptor on the cell surface (CCR5, CXCR4, or both).

Like other retroviruses, HIV copies its genetic material in a reverse manner compared with other viruses and cells. Through the action of reverse transcriptase, HIV produces deoxyribonucleic acid (DNA) from its viral ribonucleic acid (RNA). Transcription is often poor, leading to mutations, some of which make HIV resistant to antiviral drugs. The viral DNA enters the nucleus of the cell and is incorporated into the host cell’s DNA, where it’s transcribed into more viral RNA. If the host cell reproduces, it duplicates the HIV DNA along with its own and passes it on to the daughter cells. Thus, the host cell carries this information and, if activated, replicates the virus. Viral enzymes and proteases arrange the structural components and RNA into viral particles that move to the periphery of the host cell, where the virus buds and emerges from the host cell — free to infect other cells. Reservoirs of HIV include gut-associated lymphoid tissue (GALT) and peripheral lymphoid tissues. The reproductive tract, bone marrow, reticuloendothelial system, peripheral blood dendritic cells, and microglial cells of the central nervous system are sites that are believed to be reservoirs of HIV.

HIV replication may lead to cell death or the virus may become latent. HIV infection leads to profound pathology, either directly through destruction of CD4⁺ cells, other immune cells, and neuroglial cells or indirectly through the secondary effects of CD4⁺ T-cell dysfunction and resulting immunosuppression.

During primary exposure to an allergen, T cells recognize the foreign allergens and release chemicals that instruct B cells to produce specific antibodies called IgE. IgE antibodies attach themselves to mast cells. Mast cells with attached IgE can remain in the body for years, ready to react when they next encounter the same allergen.

The second time the allergen enters the body, it comes into direct contact with the IgE antibodies attached to the mast cells. This stimulates the mast cells to release chemicals, such as histamine, which initiate a response that causes tightening of the smooth muscles in the airways, dilation of small blood vessels, increased mucus secretion in the nasal cavity and airways, and itching.