JANUARY/FEBRUARY 2020. DISCOVER 43the genus Homo, though they were unable
to determine which species.
Researchers continued to excavate the
cave, eventually unearthing more bones —
plus seven teeth — from three individuals
who lived at least 50,000 years ago. That
date would mean they were alive at the
same time as Neanderthals, Denisovans
and our own species, as well as Homo flo-
resiensis, short and small-brained ancient
humans who lived in Indonesia.
The Callao Cave bones have a unique
combination of primitive and modern
human traits, leading the researchers
to classify them as an entirely new spe-
cies: Homo luzonensis.
The seven teeth found were of par-
ticular interest to the researchers. Oddly
small molars are similar in shape to
those of H. sapiens. However, they also
have features that resemble the molars
of H. erectus, a much earlier human spe-
cies that dispersed out of Africa about
2 million years ago. And parts of the pre-
molars of H. luzonensis resemble those
of H. floresiensis.Meanwhile, the curved shape of the toe
and finger bones of H. luzonensis look like
those of australopiths, human predeces-
sors that lived some 3 million years ago.
That means H. luzonensis likely spent
some of its time climbing in trees — even
though other Homo species were ground-
dwellers by this point.
The discovery of H. luzonensis on an
island that was never connected to main-
land Asia, and which would have required
a significant sea crossing to reach, adds to
the mystery surrounding the latest addi-
FRO tion to our family tree.
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UNIVERS
ITY18
Editing Out HIV
BY RONI DENGLERi
Nearly 37 million people have human immunodeficiency virus (HIV),
the cause of AIDS. The go-to treatment for the infection, antiretroviral
therapy (ART), can prevent the disease’s progression, allowing people
to live longer and healthier lives. But even with ART, the virus still lingers in
the body by copying itself into the DNA of infected cells.
This year, researchers described a new form of ART which, in combina-
tion with CRISPR gene editing, eradicated the virus during testing on mice
— a big step toward new therapeutic avenues for HIV patients.
To mimic a human infection in mice, the researchers used “humanized
mice,” which make human immune cells, rather than mouse immune cells.
These human cells are susceptible to HIV. When the team injected the
mice with the virus, they saw the infection take up residence in the places
it would in humans: in DNA in cells in the lymph nodes, spleen, liver, lungs
and brain.
The team used the mice to test a new, so-called “long-acting slow-
effective release” (LASER) ART treatment. The therapy uses retroviral
nanoparticles that take more time to dissolve and persist longer in the
body, to prevent the virus from replicating. They found that LASER ART,
administered every few weeks rather than daily, stopped 99 percent of the
virus’ replication. But, as with standard ART, the new treatment could not
remove any part of the virus that had already entered a patient’s DNA.
So for the final punch, the researchers used CRISPR gene editing to cut
out the virus’ DNA from the genomes of the infected mice. This eliminated
all traces of HIV from more than 30 percent of the mice, the team reported
in July in the journal Nature Communications.
“Our findings show for the first time that HIV can be cured from an
infected cell and the cell will remain virus-free,” said Temple University
virologist Kamel Khalili, one of the senior investigators leading the research.
He says the results show promise for moving ahead within a couple of
years to trials in non-human primates and, eventually, to humans.Temple University virologist Kamel Khalili (front center) and a team of researchers showed
that CRISPR gene-editing technology could help remove HIV from the cells of infected mice.Philip Piper