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Like other budding band nerds across the country, I spent the summer before my freshman year of high school learning how to march in formation while playing my clarinet.

In those weeks under the relentless Houston sun, I was the picture of health. Gapped-toothed, skinny and tan, I could endure hours of drills soundtracked by (not very good) performances of Electric Light Orchestra’s “Evil Woman.”

Our band director, Mr. C, was also skinny and tan. He had a long fuse for teenagers’ antics. I guess you have to when you’re in that line of work. But you could tell the heat was too much for him sometimes. I don’t know how he managed to bear it while dying of AIDS. 

This was 1992. The red ribbon had just emerged as a symbol for HIV/AIDS. Queen front man Freddy Mercury had been dead less than a year. And antiretrovirals hadn’t made it to the bedside yet.

Fear of the virus and discrimination against those with it were so severe that the International AIDS Conference had to be moved from Boston to Amsterdam because the U.S. would not allow people with HIV into the country. 

I was oblivious to it all.

I don’t remember Mr. C ever coming out and saying directly that he had AIDS, although he must have. I do recall sitting, legs crossed, on the floor of the band hall when he told us he was sick and wasn’t going to get better. He asked us if we had any questions, and one student asked how it happened.

“I’m a 40-year-old man,” Mr. C said. “I’ve been around the block.” He died not long after.

By the time I graduated from high school, HIV infections worldwide had more than doubled, rising to an estimated 23 million. Janeane Garofalo’s character in the 1994 film “Reality Bites” captured that time this way: “The free clinic AIDS test. The rite of passage for our generation.”

Fast forward to the late 2000s. I was a young professional when a friend, then in his mid-30s, told me he’d tested positive for HIV. I didn’t know what the diagnosis meant for him. I was afraid he was dying like Mr. C. 

I stammered and admitted that I was at a loss. He assured me that testing positive was no longer necessarily a death sentence.

About a year later, the U.S. lifted the HIV travel ban.

A decade later, my friend is doing just fine.

June 27 is National HIV Testing Day. Many thanks to science communicator Jonathan Griffin for pulling together the snapshot below of HIV/AIDS research as it stands today.

When HIV drugs don’t cooperate

Drugs are considered synergistic if their effectiveness together is greater than the sum of their effects. That is, a drug that is synergistic with another not only performs a beneficial function itself but also makes the second drug perform its function better. Researchers at Thomas Jefferson University studying combinations of drugs against HIV have discovered that varying factors in patients and in the virus affect whether drugs used together act synergistically or not. .

Slowing the viral production line

Preventing HIV-1 replication in infected patients is crucial for treatment. The long terminal repeat region of HIV-1 promotes transcription of the viral DNA and represents a potential target for antiviral therapy. , a team of researchers in China revealed that the protein SAFB1 prevents reactivation of HIV by blocking RNA polymerase II from accessing the long terminal repeat and initiating transcription of the viral DNA.

Why one kind of HIV-1 reigns supreme

There are several subtypes of HIV-1, but subtype C stands out as it causes about half of all infections globally. Why is this type so dominant? Researchers have hypothesized it’s because duplicated copies of the amino acid sequence PTAP enhances replication. To uncover how PTAP motifs confer an advantage to HIV-1C, researchers in India studied a group of HIV patients over three years. In a , they suggest that viral strains with multiple PTAP motifs dominate because the motifs increase association with TSG101, a protein that helps the virus exit the cell.

Targeting semen amyloid fibrils to reduce HIV infectivity

Infection-promoting amyloid fibrils have been observed in the semen of both healthy and HIV-infected men. Researchers are interested in identifying compounds that disrupt the formation of these fibrils or rid them of their infectivity-enhancing properties. One team  that gallic acid shows promise.

Rearranging the immune system

To replicate and survive, HIV-1 makes significant changes in the host immune system. But these alterations have not been studied at the protein level. , researchers at the University of Zurich used mass spectrometry to find how HIV-1 modulates proteins in human T cells. They found that TLR-4 signaling, which is central to T cell receptor signaling in mice, decreased over time as expression of viral protein increased. The authors suggest that further investigation of these perturbations could help identify future therapeutic targets.

Resistance in women at risk

Biological factors might influence how susceptible an individual is to HIV infection, and, in some cases, offer natural resistance. To unveil potential markers for resistance, researchers studied genital protein signatures of uninfected women with HIV-positive sexual partners.  show that these uninfected woman had higher levels of proteins related to epithelial function and inflammation.

The catch-22 of antiretroviral therapy

The cholesterol carrying lipoprotein (a), or Lp(a), is an established risk factor for cardiovascular disease. In this , a team of researchers show that HIV induces suppression of Lp(a) levels, however, this effect is undone by treatment with antiretroviral therapy, increasing risk of cardiovascular disease in HIV-positive patients.

An antibody barricade prevents HIV infection

Lipid rafts are cholesterol-rich domains on the surface of cell membranes that play a key role in HIV-1 entry. Some naturally occurring antibodies are able to bind specifically to cholesterol, and a team of researchers in Hungary aimed to find out if they could interrupt HIV infection.  that a certain kind of anticholesterol antibody triggers lateral clustering of lipid rafts and prevents HIV production in both human macrophages and T cells.