HIV is a retrovirus, specifically a lentivirus. That classification tells you two important things about how it behaves: it converts its genetic material from RNA into DNA (the “retro” part, since this reverses the normal flow of genetic information), and it causes slow, progressive disease over many years (the “lenti” part, from the Latin word for slow). HIV belongs to the family Retroviridae, and it’s one of the most studied viruses in history.
What Makes a Retrovirus Different
Most viruses carry either DNA or RNA and use it directly to reproduce. Retroviruses do something unusual. HIV carries its genetic code as single-stranded RNA, but once inside a human cell, it uses a special enzyme to convert that RNA into DNA. That newly made DNA then gets inserted directly into the infected cell’s own genome, essentially stitching itself into your chromosomes. This is why HIV infection is permanent: the viral blueprint becomes part of your cells’ genetic code, and your body has no way to remove it.
The enzyme responsible for this RNA-to-DNA conversion is called reverse transcriptase, and it’s a defining feature of all retroviruses. HIV also carries two other key enzymes. One (integrase) handles the job of splicing viral DNA into the host cell’s chromosomes. The other (protease) cuts newly made viral proteins into their functional shapes so new virus particles can mature and become infectious. All three of these enzymes are targets for modern HIV medications.
The Physical Structure of HIV
An HIV particle is roughly spherical, about 100 to 120 nanometers across. That’s far too small to see with a regular microscope. On the outside, it’s wrapped in a lipid envelope stolen from the last human cell it budded out of. This stolen membrane even carries some human proteins, which helps the virus partially camouflage itself from the immune system.
Studding that envelope are mushroom-shaped protein spikes made of two components: a surface protein (gp120) and a transmembrane anchor (gp41). These spikes are what the virus uses to latch onto and enter new cells. The surface protein is heavily coated in sugar molecules, covering more than half its surface in a carbohydrate shield sometimes called the “silent face” because it blocks antibodies from recognizing the virus. Inside the envelope, a cone-shaped capsid core built from roughly 1,500 protein subunits encloses two copies of the viral RNA genome, which is about 9,200 genetic letters long.
How HIV Gets Into Cells
HIV specifically targets immune cells that carry a surface marker called CD4, most importantly a type of white blood cell known as a CD4 T cell. These cells coordinate much of the immune response, which is why losing them is so devastating. But CD4 alone isn’t enough for the virus to get in. HIV also needs a second receptor on the cell surface, either CCR5 or CXCR4, to complete the entry process.
These two co-receptors sit on different subsets of T cells. CCR5 is found mainly on activated memory T cells, the ones that have encountered infections before. CXCR4 appears predominantly on naive T cells, those that haven’t yet been activated. Different strains of HIV prefer different co-receptors, which influences which immune cells get hit hardest at various stages of infection. Early in the course of disease, HIV strains that use CCR5 tend to dominate. Some people carry a genetic mutation that disables CCR5, giving them substantial natural resistance to infection.
The Seven-Stage Life Cycle
HIV reproduces through a well-defined sequence. First, the virus binds to a CD4 receptor, then engages a co-receptor. This triggers the viral envelope to fuse with the cell membrane, dumping the viral contents inside. Once in the cell, reverse transcriptase converts the RNA genome into DNA. Integrase then inserts that DNA into the cell’s chromosomes. From there, the cell’s own machinery reads the viral instructions and produces long chains of viral proteins. These proteins, along with new copies of viral RNA, migrate to the cell surface and assemble into immature virus particles that bud off from the cell. Finally, protease cleaves the protein chains into their active forms, producing a mature, infectious virus ready to infect the next cell.
Each infected cell can produce thousands of new virus particles. Without treatment, HIV generates billions of new copies per day, and because reverse transcriptase is error-prone, each generation introduces mutations. This extraordinary mutation rate is a major reason the virus evades immune responses and why combination drug therapy, hitting multiple stages of the life cycle at once, is necessary for effective treatment.
Two Types: HIV-1 and HIV-2
There are actually two distinct species of HIV. HIV-1 is responsible for the vast majority of infections worldwide and is what people generally mean when they say “HIV.” HIV-2 is found primarily in West Africa and in countries with historical ties to that region, particularly Portugal, Spain, France, Angola, Mozambique, Brazil, and parts of India.
HIV-2 is notably less aggressive. People with HIV-2 typically have lower levels of virus in their blood, lose CD4 cells more slowly, and take longer to develop AIDS. It also spreads less efficiently. In studies from West Africa conducted before antiretroviral therapy was available, perinatal transmission of HIV-2 was under 5%, compared with roughly 25% for HIV-1. Sexual transmission is also less efficient with HIV-2. That said, HIV-2 can still cause AIDS and still requires treatment.
HIV-1 itself is divided into four groups. Group M (for “major”) is behind the global pandemic and shows the greatest genetic diversity, with numerous subtypes circulating in different regions. Groups N and O are uncommon, and Group P is extremely rare. These groups reflect separate cross-species transmission events from primates to humans.
Where HIV Came From
HIV is a zoonotic virus, meaning it jumped from animals to humans. HIV-1 originated from simian immunodeficiency viruses (SIVs) carried by chimpanzees and gorillas in Central Africa. The most widespread and dangerous form, HIV-1 Group M, evolved from a chimpanzee virus (SIVcpz), while the rare Group O traces back to gorillas (SIVgor). HIV-2 has a separate origin entirely, arising from SIV strains found in sooty mangabey monkeys in West Africa.
Dozens of other SIV strains circulate in various primate species, but despite frequent human contact with these animals, there’s no evidence of sustained human transmission from those other viruses. The jump from primate to human required the virus to overcome significant biological barriers, including differences in immune defense proteins and cell surface receptors between species. The few successful crossover events that did occur gave rise to the HIV strains we know today.