HIV-1 is the most common type of human immunodeficiency virus, responsible for about 95% of all HIV infections worldwide. It’s the virus behind the global AIDS pandemic, and when people say “HIV” without specifying a type, they almost always mean HIV-1. A second type, HIV-2, exists but is far less common and largely confined to parts of West and Central Africa.
How HIV-1 Differs From HIV-2
There are two distinct species of HIV, and they behave quite differently inside the body. HIV-1 is more aggressive. It replicates faster, produces viral loads roughly 28 times higher than HIV-2, and depletes immune cells at about twice the rate. People with untreated HIV-1 typically develop AIDS within about 6 years, compared to roughly 14 years for HIV-2. The asymptomatic period before any symptoms appear averages 8.2 years for HIV-1 versus 15.6 years for HIV-2.
HIV-1 also spreads more efficiently. Mother-to-child transmission rates range from 15% to 30% with HIV-1, compared to just 1% to 2% with HIV-2. This difference in transmissibility is a major reason HIV-1 spread globally while HIV-2 remained mostly regional. Around 2 million people live with HIV-2 today, nearly all in West and Central Africa.
Genetic Subtypes of HIV-1
HIV-1 is divided into four groups: M, N, O, and P. Group M (for “major”) is by far the most significant, containing the subtypes responsible for the vast majority of infections worldwide. Groups N, O, and P are rare and mostly found in Central Africa.
Within Group M, there are nine distinct subtypes. The three most common globally are subtype C (accounting for about 23% of infections), subtype A (about 17%), and a recombinant form called CRF01_AE (roughly 10%). Subtype B, which dominates in the Americas and Europe, makes up about 8.5% of global infections. These subtypes matter because they can influence how the virus responds to certain treatments and diagnostic tests, though modern therapies work across all subtypes.
How HIV-1 Infects the Body
HIV-1 targets a specific type of immune cell called a CD4 cell. These cells coordinate your immune response, essentially acting as the command center for fighting infections. The virus hijacks them through a seven-step process.
First, HIV-1 attaches to receptors on the surface of a CD4 cell and fuses with its membrane to get inside. Once in, the virus uses an enzyme called reverse transcriptase to convert its own genetic material (RNA) into DNA, a format the human cell can read. Another viral enzyme, integrase, then stitches that viral DNA directly into the cell’s own DNA. At that point, the cell has been permanently reprogrammed. Every time it divides, it produces new copies of the virus alongside its normal functions.
The cell builds new viral proteins and assembles them into immature virus particles that push out through the cell surface. A third enzyme, protease, then cuts these proteins into their final shape, creating mature, infectious virus particles ready to infect more CD4 cells. This cycle repeats billions of times per day in an untreated person.
Stages of HIV-1 Infection
Without treatment, HIV-1 infection progresses through three broad stages, tracked largely by the number of CD4 cells in a drop of blood. A healthy person typically has more than 500 CD4 cells per microliter.
During acute infection, which occurs in the first few weeks after exposure, the virus replicates rapidly and CD4 counts may temporarily drop. Many people experience flu-like symptoms: fever, sore throat, swollen glands, rash, or muscle aches. These symptoms are easy to mistake for another illness and usually resolve on their own, even as the virus continues spreading through the body.
The second stage is clinical latency, sometimes called the chronic stage. The virus is still active but reproduces at much lower levels. People in this stage may feel fine for years. As CD4 counts gradually decline (at a rate of roughly 0.9% per year with HIV-1), the immune system weakens. When CD4 counts drop into the 200 to 499 range, people become more vulnerable to infections like shingles, persistent yeast infections, and prolonged fevers or diarrhea.
AIDS is diagnosed when CD4 counts fall below 200 or when certain serious infections appear. These include specific types of pneumonia, tuberculosis, certain cancers like Kaposi’s sarcoma, and a wasting syndrome. At this stage, the immune system is severely compromised and can no longer fight off infections that a healthy body would easily handle.
How HIV-1 Spreads
HIV-1 transmission risk varies enormously depending on the type of exposure. The highest-risk route is blood transfusion with infected blood, which carries a 92.5% chance of transmission per event, though modern blood screening has made this exceedingly rare in most countries.
For sexual contact (without condom use and with an infected partner), the risk per single act breaks down like this:
- Receptive anal intercourse: roughly 138 per 10,000 exposures (about 1.4%)
- Insertive anal intercourse: about 11 per 10,000 (0.11%)
- Receptive vaginal intercourse: about 8 per 10,000 (0.08%)
- Insertive vaginal intercourse: about 4 per 10,000 (0.04%)
- Oral sex (giving or receiving): very low, between 0 and 4 per 10,000
Sharing needles during injection drug use carries a risk of about 63 per 10,000 exposures (0.63%). Mother-to-child transmission, which can happen during pregnancy, birth, or breastfeeding, occurs in 15% to 30% of cases without treatment. These numbers represent averages. Factors like viral load, the presence of other sexually transmitted infections, and whether the infected person is on effective treatment all shift the risk significantly. A person on treatment with an undetectable viral load effectively cannot transmit the virus sexually.
Testing and Detection Windows
How soon HIV-1 can be detected depends on the type of test. The fastest option is a nucleic acid test, which looks for the virus’s genetic material directly. It can detect HIV as early as 5 to 10 days after exposure, making it useful when acute infection is suspected.
Fourth-generation antigen/antibody tests are the standard in most clinical settings. These detect both HIV antibodies and a viral protein called p24, which appears early in infection. The p24 protein can show up as early as 14 days after exposure. Most people will test positive within 3 weeks using this type of test, though some take up to 3 months to produce a positive result.
Rapid antibody tests, which detect only the body’s immune response to the virus, can identify infection roughly 3 weeks after transmission. Because they miss the earliest window of infection, a negative rapid test after a recent exposure should be followed up with a more sensitive test.
How HIV-1 Is Treated
HIV-1 is treated with antiretroviral therapy, a combination of drugs that target different steps in the virus’s life cycle. The current standard for most newly diagnosed people is a regimen built around a second-generation integrase inhibitor (which blocks the virus from inserting its DNA into your cells) combined with two drugs that block reverse transcription (the step where the virus converts its RNA into DNA).
These combination regimens are highly effective. They reduce the amount of virus in the blood to undetectable levels in most people, allowing CD4 counts to recover and the immune system to rebuild. Treatment is lifelong because HIV-1 integrates into the DNA of long-lived cells, creating a hidden reservoir the immune system cannot clear. Stopping treatment allows the virus to rebound from these reservoirs.
Other drug classes exist for people who develop resistance or can’t tolerate standard regimens, including protease inhibitors (which prevent new virus particles from maturing), fusion inhibitors (which block the virus from entering cells), and newer options that target the virus’s outer shell. With consistent treatment, people living with HIV-1 now have a near-normal life expectancy.