Scientific American - USA (2020-10)

40 Scientific American, October 2020

proteins also inhibit our own cells. The difference be -

tween a concentration in which the drug inhibits the

virus target and a concentration in which it hurts the

human proteins is called the therapeutic index. The

therapeutic index gives you the window in which the

drug will be effective against the virus without causing

undue side effects. That window is rather narrow for all

polymerase and protease inhibitors.

The gold standard for AIDS treatment now is called

antiretroviral therapy—essentially patients take a cock-

tail of at least three different drugs that attack the HIV

virus in different ways. The strategy is based on earlier

success we had in fighting cancer. In the late 1970s I

established a laboratory at Harvard University’s Dana-

Farber Cancer Institute to develop new drugs to treat

cancer patients. Cancers developed resistance over time

to single drugs, but combinations of drugs were effec-

tive in slowing, stopping or killing the cancers. We took

that same lesson of combination chemotherapy to HIV.

By the early 1990s the first combination AIDS treat-

ments were saving the lives of people infected with HIV.

Today an infection is far from the death sentence it used

to be—patients can now live almost unaffected by HIV,

with a relatively minimal impact on life expectancy.

We already know resistance to single drugs will be -

devil COVID-19 treatments. We have seen resistance to

single, anti-SARS-CoV-2 drugs develop rapidly in early

lab studies. Just as with AIDS and cancer, we need a

combination of medicines to treat this disease. The goal

of the biotechnology and pharmaceutical industries now

is to develop an array of highly potent and specific drugs,

each of which targets a different function of the virus.

Decades of research on HIV has shown the way and gives

us confidence in our eventual success.

HUMAN BEHAVIOR

in trying to undErstand and counter the AIDS epidem-

ic, physician and virologist Robert Redfield (who is now

head of the Centers for Disease Control and Preven-

tion) and I became good friends in the early 1980s. We

quickly learned that while many politicians across the

globe refused to recognize HIV as a threat to their pop-

ulations, militaries were an exception. Nearly all coun-

tries considered AIDS a serious danger to troops and

military readiness and a potentially huge drain on fu-

ture military funds. Their view was, “Let’s not blind

ourselves and pretend soldiers are saints. They are not.

They are humans.” Redfield, then at Walter Reed Army

Medical Center, helped to design and manage a pro-

gram to test the entire U.S. uniformed forces for HIV

infection (although the consequences of this test were

controversial, and recruits who tested positive were

barred from service).

At the time there were no effective drugs; the disease

killed more than 90  percent of those infected. When

married couples were tested and one partner was infect-

ed and one not, doctors advised them in the strongest

possible terms to use condoms. I was stunned to learn

that fewer than a third complied with the advice. “If

people don’t respond to the lethal danger of unprotect-

ed sex with their husband or wife, we are in real trou-

ble,” I thought. Over the next five years more than three

quarters of the uninfected partners contracted HIV.

I have always used this experience as a guide to pit

hope against reality. Human sexuality—the drive for sex

and physical connection—is deeply embedded in our

nature. I knew in the 1980s it was very unlikely people

would change their sexual behavior in a major way. In

the 19th century everyone knew how syphilis was

contracted and that it was serious disease. Yet syphilis

still infected at least 10  to 15  percent of American citi-

zens at the beginning of the 20th century. It was not

that people were ignorant of how to catch it; it is that

they did not change their lifestyle accordingly.

There is likewise a sexual dynamic to COVID-19 that

often goes unmentioned. It is part of what is driving

people out of their homes and into bars and parties.

Anyone with a craving for a beer can quench their thirst

in the safety of their own home, but gratification comes

less easily for other desires, especially when one is

young, single and living alone. Our public health strat-

egies should not ignore this fact.

The same lessons we learned in the midst of the HIV

epidemic to help young people change their behaviors

apply today to COVID-19: know your risk, know your

partners and take necessary precautions. Many young

people operate under the false assumption that even if

they become infected, they will not become severely ill.

Not only is this belief untrue, but even people with

asymptomatic infections can suffer serious, lasting

damage. But the more people understand the risk—

younger people especially—the greater likelihood they

will take the steps necessary to protect themselves and

others. We saw this happen with AIDS.

FUNDING

whEn i ask world ExpErts what they know about the de-

tailed molecular biology of SARS-CoV-2 or, for that mat-

ter, any other coronavirus, they do not have the kind of

answers they should. Why? Because governments and

industry pulled the plug on coronavirus research funding

in 2006 after the first SARS (severe acute respiratory syn-

drome) pandemic faded away and again in the years im-

mediately following the MERS (Middle East respiratory

syndrome, also caused by a coronavirus) outbreak when

it seemed to be controllable. Funding agencies everywhere,

not just in the U.S. but in China, Japan, Singapore, Hong

Kong and the Middle East—countries affected by SARS

and MERS—underestimated the threat of coronaviruses.

Despite clear, persistent, highly vocal warnings from many

Just as with AIDS and cancer,

we will need a combination of

medicines to treat this disease.

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