Final answer:
The CCR5-delta 32 mutation results in a missing protein on cell surfaces, providing significant resistance to HIV infection due to the virus's inability to bind and enter CD4+ helper T cells. As for treatment, antiretroviral drugs target viral replication, and an effective HIV vaccine remains elusive due to rapid viral mutations.
Step-by-step explanation:
The missing protein that individuals lack on the surface of their cells, which makes them almost never infected with HIV despite multiple sexual contacts with an infected partner, is the CCR5 receptor. More specifically, these individuals have the CCR5-delta 32 mutation which prevents the expression of the normal CCR5 protein on the cell surface. HIV-1 requires the presence of the CCR5 receptor, in addition to the CD4 receptor, on the host's immune cells to gain entry and establish infection. When the CCR5 receptor is absent or malformed due to the mutation, the virus is unable to attach to and infect the CD4+ helper T cells, dramatically reducing susceptibility to the virus.
Although no cure for HIV exists, treatment involves the use of antiretroviral drugs that target virally encoded proteins necessary for viral replication. This therapeutic approach has been successful in extending the lives of individuals with HIV. However, the development of an HIV vaccine has been a challenge due to the virus's ability to mutate rapidly, which aids in its evasion from the immune system.