A hunter in the Congo River basin killed a chimpanzee for food sometime in the 1920s. In the process of butchering the chimpanzee, he got himself covered in blood up to his elbows.
By a tragic stroke of misfortune, a whole series of events then coincided.
First, the SIV the chimp was infected with had recently recombined with another, similar virus that infected a type of small monkey called a mangabey. This happened when the chimp, or some other chimp, caught and ate a monkey.
Something about the genome of that recombined virus made it more capable of easily infecting humans, and also more deadly.
Also, the hunter had injured himself. Maybe he slipped and cut himself on rocks during the chase. Maybe he accidentally sliced open a finger cutting the chimp up.
However it happened, he got a lot of chimp blood into his new, open wound.
SIV viral particles (virions) found their way from capillaries to veins. They did what these virions do. They sought out CD4 white blood cells and took them over to turn them into virus reproduction factories.
Most of them failed. The human cells weren’t quite what they needed. They couldn’t get in. They died.
But a few virions, or maybe even just one, were a little tiny bit different. They were adapted enough to successfully invade human CD4 cells.
The virions they later spit out were all adapted the same way.
HIV-1 was born.
The hunter returned to his village, roasted the chimp, hosted a feast, and later retired to have sex with his wife.
After a while, she had HIV in her bloodstream too.
And that’s how it all started.