The human immunodeficiency virus (HIV) belongs to the family of viruses known as retroviruses.
In order to infect host cells HIV must first bind to a cell surface receptor (a CD4 antigen), and a co-receptor (CCR5) found on cells that present antigen material on the surface of some immune cells:
- helper T-cells (T-lymphocytes),
- monocytes,
- macrophages and
- dendritic cells (immune cells that process and present or display antigen material) and glial cells (a type of nerve cell).
Presentation of foreign antigen material allows other immune cells the opportunity to recognize that threats to the host. Antigen material is displayed on the cell surface much like a hunter displays trophies over the fireplace. These trophies are recognized by cytotoxic T-lymphocytes so that they can be targeted and destroyed by other immune cells. The situation is ironic considering that the whole purpose of the immune system is to protect us against these same threats!
Trophies presented on the cell surface allow detection of foreign antigen material so that infected and defective cells can be targeted and destroyed by other immune cells. Cytotoxic T-lymphocytes attempt to recognize virus infected cells and destroy them, and the viruses contained.
A glycoprotein on the HIV particle binds to CD4 and CCR5 becoming a key to a lock on the cell surface, allowing cell entry. Of course, this mechanism is meant as an immune defence to detect, bind and inactivate the virus, and at the same time initiate additional immune responses to protect the host from this specific threat.
However, HIV uses the host's metabolic machinery, and the host protein processing and cell reproduction mechanisms to replicate rapidly and infect other cells: each viral particle captured by an immune cell, further replicates using the newly infected cell’s metabolic machinery, generally without influencing normal cell operation.
The irony here is that the purpose of these immune cells is to protect us against just such threats!
Gene mutations have been identified in some individuals that prevent CD4 receptor attachment so that the virus cannot gain entry.
Countering immune responses, viruses evolve to side-step inhibition processes initiated by the host immune system. The rapid rate of viral replication produces huge numbers of off-spring, many of which will be unable to gain entry to host cells.
However, even if only one or two mutants capable of adapting to immune defences were to be successful in gaining entry to the cell, rapid replication would soon provide a whole new generation of viral particles capable of side-stepping the host’s immune defences. A complex game of chess ensues in which the immune system and the virus attempt to conquer each other. Similarly, a game of War rages when anti-viral agents threaten the survival of the HIV.
Recently, genetic make-up has also been found to influence protection against the human immunodeficiency virus (HIV) and other foreign invaders. Individuals who carry the gene for expression of HLA-B57 antigens have been shown to have much slower HIV-1 (human immunodeficiency virus type -1) disease progression than individuals who do not express HLA-B57.
Read more about HIV infection and protection:
HIV Protection: CCR5 Chemokine Receptor Mutation
Resistance to Anti-viral Agents: Mutations Side-step Inhibition Processes
Antiviral Therapy: Introduction to Antiviral Therapy
Antiviral Agents: Classes of Anti-viral Medications
