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Extracts of 28 species of marine macroscopic algae collected from various coastal habitats of northern California were examined for antiviral activity against a broad spectrum of mammalian viruses. Ten members of Rhodophyta contained substance(s) which caused greater than a 2 log reduction in the infectivity of herpes simplex virus types 1 and 2. In addition, anti‐Coxsackie Bs virus activity was detected in extracts of Constantinea simplex Setchell. The physical and chemical properties of the substance in extracts of Farlowia mollis (Harvey and Bailey) Farlow and Setchell and C. simplex indicated the active agent was a structural polysaccharide.

Extracts from two species of marine red algae, Cryptosyphonia woodii and Farlowia mollis, specifically inhibited herpes simplex virus replication in vitro.Studies on marine flora and fauna as sources of antiviral agents have not been extensive (1, 5) despite indications that such sources were potentially useful (2, 4, 7). This preliminary report describes the inhibition of types 1 and 2 herpes simplex virus (HSV-1 and HSV-2) replication in cell monolayers pretreated with extracts derived from two related species of Rhodophyta, Cryptosyphonia woodii and Farlowia mollis.Algae were collected at Duxbury Reef, Bolinas, Calif., identified by species, and stored at -70 C. Frozen samples were combined with citrate-phosphate buffer (3) at pH 7.0 (20%, wet wt/vol), homogenized in a Waring blender, and then incubated at 4 C overnight.Antiviral activity was assessed as follows.

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Coinfected mice were examined for a possible interaction between the scrapie agent and an adenovirus. A low titer (10² TCD₅₀) of mouse adenovirus (MAdV) caused a significant acceleration of clinical signs of scrapie in mice infected 128 days previously with scrapie. In this experiment, the coinfected mice died 19 days earlier than mice infected with scrapie alone. When a higher titer of MAdV (10⁴–10⁵ PFU) was used, a more drastic acceleration of scrapie disease was seen in mice infected 85 and 110 days previously with scrapie. At 85 days, coinfection caused mice to die 37 days earlier than mice infected with scrapie alone, whereas at 110 days, coinfection caused mice to die 52 days earlier than mice infected with scrapie alone. MAdV alone caused no clinical disease in normal mice. The brains of coinfected mice and mice that had been infected with scrapie alone showed a histopathology consistent with scrapie. A possible explanation for these findings is that the replication of the scrapie agent is accelerated by adenovirus. Defective parvoviruses are known to be helped by adenoviruses. Spleens from coinfected mice but not from mice infected with MAdV alone yielded, in cultures of BALB 3T3 cells, infectious MAdV and one or two smaller agents with the dimension and shape of a parvovirus.