Wednesday, May 18, 2022

The Impact of Sunscreen Products Upon the Viability of Coral

It has been reported that the compound oxybenzone (shown below) that is the active ingredient in sunscreen preparations exhibits a toxicity to corals. The mechanism of this toxicity has not been fully understood.


William Mitch and his colleagues at Civil and Engineering at Stanford University, California have successfully delineated the mechanisms involved in regard to this toxicity. They have established that oxybenzone caused increased mortality of a sea anemone under conditions that simulated the natural (UV) radiation (290 to 370 nanometers). Furthermore they found that both the anemone and a mushroom coral formed oxybenzone–glucoside conjugates (see image below) that were powerful auto-oxidants. Corals are composed of layers, of calcium carbonate secreted by soft bodied animals called coral polyps. These polyps live in a symbiotic relationship with a host zooxanthellae such as algae that gives the coral its color. Corals devoid of algae are bleached as a consequence of climate change.

Algal symbionts took up these conjugates, and their mortality correlated well with the corresponding concentration of oxybenzone glucosides within the animal cells. Since many commercial sunscreens preparations contain compounds structurally analogous to oxybenzone, an understanding of the mechanism of this toxicity should enable the synthesis of more eco-friendly sunscreen products.

According to the authors of a paper published in a recent article in the prestigious journal, Science, “Research in the US Virgin Islands found no substantial settlement of coral larvae, survival of juvenile corals, or regeneration of adult tissue in induced lesions over a 5-year period in Trunk Bay, where high levels of recreational swimming resulted in up to 1.4 mg of oxybenzone per liter of seawater. Meanwhile, a thriving coral community was found at neighboring Caneel Bay, with lower recreational use but presumably the same impacts from global stressors. Exacerbation of coral declines by sunscreens washed off tourists would be ironic and particularly pernicious, given the promotion of ecotourism in the interest of protecting coral reefs.”

Finally, the authors go on to say that, “With recent moves by regulatory authorities in Hawaii and elsewhere to ban oxybenzone, understanding the mechanism(s) of its phototoxicity is important to ensure that the sunscreen components that are selected as alternatives are truly safer for corals.”

The ecological factors that promote and sustain the delicate balance in the natural world can easily be disrupted by human encroachment. It is vitally important to support the kind of scientific investigations that uncover these human factors and find ways to mitigate their impact.

Sunday, May 15, 2022

The Filovirus

One of the suspected and postulated origins of COVID-19 virus in human populations is the transfer of the virus across the species barrier i.e. from bats. This capacity to “jump” across species is of added concern given the severity of illness originating from human infection by a family of viruses referred to as filoviruses. A filovirus is a filamentous RNA virus (see image below).


Infection by this virus is the causative agent of so-called “hemorrhagic fevers” in humans and primates, that includes the Ebola and Marburg viruses. These viruses can result in multiple organ system involvement. The Marburg virus, for example, can produce nausea, vomiting, chest pain, a sore throat, abdominal pain, and diarrhea may appear. Symptoms become increasingly severe and can include jaundice, inflammation of the pancreas, severe weight loss, delirium, shock, liver failure, massive hemorrhaging, and multi-organ dysfunction. These diseases are most prevalent in sub-Saharan Africa.


In 2002, the Lloviu filovirus was found in Schreiber bats (Miniopterus schreibersii) in northern Spain. This infection resulted in a massive die-off of these animals. Gabor Kemenesi and his colleagues from the National Laboratory of Virology at Szentagothai Research Center at the University of Pecs, Hungary successfully isolated and sequenced the Lloviu filovirus from Schreiber bats in Hungary. During a active surveillance of these bats, they found the Lloviu virus resident in these dead and living cave-dwelling bats.

Furthermore, antibody testing detected nine seropositive bats out of 74 live bats and four positives among 351 live bats sampled. The Lloviu virus is known to infect human cells in culture, but unlike the Ebola virus appears to be nonpathogenic to humans, at least for the time being.

Sunday, January 23, 2022

Epstein Barr Virus Infection May be Associated with the Onset of Multiple Sclerosis

Multiple Sclerosis (MS) is a chronic and debilitating disease that is a result of the destruction of the myelin sheath that serves as insulation for the peripheral nerves within the central nervous system (CNS).  The loss of myelin has serious implications for the patient suffering from this syndrome – it results in a gradual deterioration of motor function. 

To date the etiology of this disease has been unclear.  It has long been suggested that Infection with the Epstein-Barr virus (EBV) may be responsible for triggering the onset of MS.  In a recent issue of the prestigious publication Science (January, 2022), Kjetil Bjornevik, from the Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, has provided compelling statistical evidence that EBV infection triggers the onset of MS.  According to the author, “analyzed EBV antibodies in serum from 801 individuals who developed MS among a cohort of >10 million people active in the US military over a 20-year period (1993–2013). Thirty-five of the 801 MS cases were initially EBV seronegative, and 34 became infected with EBV before the onset of MS. EBV seropositivity was nearly ubiquitous at the time of MS development, with only one of 801 MS cases being EBV seronegative at the time of MS onset. These findings provide compelling data that implicate EBV as the trigger for the development of MS.” 

EBV (see diagram below) preferentially attacks B cells; B cells are the part of the immune system repertoire responsible for the production of antibodies.   In MS the myelin sheath is degraded through an inflammatory response.  It has been shown that in MS the B cells responsible for this inflammatory are derived from plasmablasts that are generated in the marrow and take residence inside the brain and its internal lining.  These plasmablasts divide and produce clusters of daughter cells that produce immunoglobulins.  These immunoglobulins contain specific antibodies that target myelin-producing glial cells within the central nervous system (CNS).

EBV Virus

One of the accepted therapies that attempt to take advantage of this etiology is the use of monoclonal antibodies that target CD20 - a protein preferentially found on the surface of B cells.  However, it has significant drawbacks in so far as these monoclonals do not readily pass through the blood brain barrier (BBB) and they are unable to bind to plasmablasts.

What remains unclear, however, is the mechanism through which EBV triggers this sequence of events in MS patients.  One possibility involves what is referred to as molecular mimicry in which some EBV proteins may be similar enough in structure to myelin that the immune system is induced to produce antibodies against the infected individual’s myelin and CNS antigens – this would represent an autoimmune response.  In addition, EBV encodes an interleukin-10–like protein, which activates B cells.  The author of this study, reports that recent evidence seems to suggest that molecular mimicry may be the actual mechanism underlying the association between EBV infection and MS.

The results of these kind intensive studies of the etiology of MS are extremely important in that the product of this work may finally produce effective therapies for MS patients.