HIV virus suppresses virus in humanized mice

A team of Yale researchers tested a new chemical compound that suppresses HIV, protects immune cells, and remains effective for weeks with a single dose. In animal experiments, the compound proved to be a promising new candidate to enhance current HIV treatment regimens-without increasing toxic side effects.

The finding builds on the work of senior co-authors Karen S. Anderson and William L. Jorgensen, who used computational and structure-based design methods to develop a class of compounds that target a viral protein essential for HIV to replicate.

The researchers refined this class of compounds to boost potency, lower toxicity, and improve drug-like properties in order to identify a promising preclinical drug candidate. In collaboration with Priti Kumar's lab at Yale, the drug candidate was tested in mice with transplanted human blood cells and infected with HIV.

In the humanized mice, the compound achieved key goals of HIV treatment: It suppressed the virus to undetectable levels in the blood; it protected the immune cells that the virus infects; and it worked synergistically with approved HIV medications, the researchers said.

Additionally, working with Yale drug delivery expert Mark Saltzman and his laboratory, the researchers found that the effects of a single dose of the compound, delivered in a long-acting nanoparticle form lasted for a month. The compound has potential for improving treatment for HIV.
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Reasons for deadly resistance in lung cancer and melanoma

Researchers have discovered why some lung cancer and melanoma develop deadly resistance to targeted therapies.
 Intricate DNA sequencing tests was performed on single cells using genetic models of lung cancer and melanoma.

Lung cancer and melanoma are amongst the hardest to treat of all the cancers because of their capacity to change their genetics and developing resistance to targeted therapies.

 Researchers used animal models from tumours derived from patients and single-cell genomics to develop a hypothetical model of resistance, known as "fitness threshold model," that shows why and how resistance to therapy occurs in lung and melanoma cancer.

Tumours like melanoma and lung cancers can grow back shortly after therapy, but when they do they are made of genetically diverse sub-groups of malignant cell that are resistant to treatment.

The genetic diversity of the lung cancer  and melanoma tumour allow them to adapt to the treatment and resist it. The effect of a given drug with the selection of resistance-causing alterations in DNA, resulting in significant implications for the treatment of cancer patients.

The way the drugs are administered during therapy can have a critical impact on the outcome of the response to treatment; intermittent administration enables simultaneous delivery of multiple targeted therapies while maintaining lower toxicity.
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