Viruses normally seem like evil little germs; they often invade our bodies’ cells and hijack their inner machinery to mass produce viral invaders, which eventually destroy their host cells as they bust out to besiege more cells. The process repeats ad nauseam. But what if that wicked master plan could be twisted to do our bidding? What if viruses only invaded cells we wanted them to kill—like cancer cells?
…the Food and Drug Administration approved the first viral-based cancer therapy.
There’s some interesting combination therapies in the works for a variety of different tumor sites that are suggesting substantially improved response rates compared to using just one of the therapies alone. Expect to see initial read outs of these new trials in the next 2 years or so.
Last week brought the horrifying news that the Ebola virus can live in the eyeballs of survivors, even after it’s been eliminated from the rest of the body. It shouldn’t have been a surprise, though. Viruses have always hidden in parts of our bodies you’d never expect. In fact, we’re all walking virus reservoirs.
The article focuses on various catchy/alarming viruses. It mentions but largely dances around being an asymptomatic carrier. A la Typhoid Mary, the most notorious case of an asymptomatic carrier. Her story is rather sad – she continued to get jobs in kitchens because it paid better than other options.
Case Western Reserve researchers are part of an international team that has discovered that a common herpes drug reduces HIV-1 levels — even when patients do not have herpes.
Published online in Clinical Infectious Diseases, the finding rebuts earlier scientific assumptions that Valacyclovir (brand name, Valtrex) required the presence of the other infection to benefit patients with HIV-1.
The result not only means that Valacyclovir can be used effectively with a broader range of HIV-1 patients, but also suggests promising new avenues for the development of HIV-fighting drugs. This insight is particularly significant given that some forms of HIV-1 have become resistant to existing medications.
…HIV-1 can lead to the immune deficiency known as AIDS. The herpes simplex virus 2 (HSV-2) causes periodic recurrence of genital herpes lesions, which increase the likelihood that a herpes sufferer may contract HIV through intimate contact. HSV-2 outbreaks are treated with either Acyclovir or the newer generation Valacyclovir, which requires less frequent dosing.
Wouldn’t be the first time a drug showed this type of cross-reactivity. Lamivudine started as an anti-HIV drug and ended up being effective as an anti-HBV drug as well. HIV is a retrovirus and HBV is a pararetrovirus – both of which have reverse transcriptase but HBV exists as a DNA virus outside the host cell while HIV exists as a RNA virus outside the host cell. This is important because RNA is more prone to mutations (thus the viral proteins made from the viral RNA avoid the antibodies custom made by the immune system from vaccines) while DNA is more stable in structure (the antibodies are able to target the common motif of the viral proteins made from the viral DNA and kill them before they have a chance to infect the organism). This explains why we have a HBV vaccine, but not an HIV vaccine.
Recent research also suggests that the chickenpox vaccine may help with herpes. Which shouldn’t be much of a surprise – chickenpox is a form of herpes.