The source of info, for the entire study if you're interested. I only quoted what seemed to be the most pertinent bits of it: http://www.ncbi.nlm.nih.gov/books/NBK92750/
Quote from the above study, condensed into info pertinent to Marek’s Disease and similar in Chickens:
11.6.2. Antibacterial and Antiviral Properties
As noted in Section 11.1, extracts of H. perforatum have been used over thousands of years to treat cuts, abrasions, and other wounds. Its usefulness in reducing inflammation is well known, and appears to be related, at least in part, to its ability to serve as an antibacterial agent. Recent research also suggests that it is useful in combating viruses.
Antibacterial properties of H. perforatum extracts were reported by Russian scientists in 1959 (Schempp et al. 1999). The main antibacterial component was determined to be hyperforin (Bystrov et al. 1975). Studies show that hyperforin inhibits the growth of certain types of microorganisms. Growth inhibition occurred for all gram-positive bacteria tested, although no growth-inhibitory effects were seen in the gram-negative bacteria tested (Bystrov et al. 1975).
Methicillin-resistant (MRSA) and penicillin-resistant (PRSA) Staphylococcus aureus were especially susceptible to hyperforin. The MRSA strain was shown to be resistant to several types of penicillins, ofloxacin, clindamycin, erythromycin, cephalosporins, and gentamicin (Bystrov et al. 1975).
Extracts of SJW have long been regarded as being effective against various classes of viruses. Studies by Mishenkova et al. (1975) indicated that flavonoid and catechin-containing fractions of SJW are active against influenza virus.
Since 1988, the virucidal activities of hypericin extract have been investigated against many other forms of viruses (Diwu 1995).
Hypericin compounds are effective against enveloped viruses, but not nonenveloped viruses (Diwu 1995), particularly when activated by light (Carpenter and Kraus 1991; Hudson, Harris, and Towers 1993; Hudson, Graham, and Towers 1994).
Hypericin inactivates enveloped viruses at different points in the viral life cycle (Lenard, Rabson, and Vanderoef 1993). Degar et al. (1992) suggested that hypericin inactivates enveloped viruses by altering viral proteins, and not nucleic acids as targeted by antiviral nucleosides.
Hypericin also inhibits the ability of viruses to fuse with cell membranes (Degar et al. 1992; Lenard, Rabson, and Vanderoef 1993), which may explain why hypericin inactivates enveloped viruses rather than nonenveloped ones.
These promising in vitro results have begun to promote various in vivo studies of certain viruses in mice.
These include LP-BMS murine immunodeficiency viruses, murine cytomegalovirus (MCMV), Sindbis virus, Friend virus, and Ranscher leukemia virus (Hudson, Lopez-Bazzocchi, and Towers 1991; Meruelo 1993; Stevenson and Lenard 1993).
Hypericin also shows in vitro activity against influenza and herpes viruses (Tang et al. 1990), vesiculostomatitis and Sendai viruses (Lenard, Rabson, and Vanderoef 1993), and duck hepatitis B virus (Moraleda et al. 1993).
Hypericin is used to inactivate several enveloped viruses present in human blood and to treat acquired immunodeficiency syndrome (AIDS) patients (Holden 1991; Meruelo 1993).
Working with the human immunodeficiency virus (HIV), Degar et al. (1992) observed changes in the p24 protein and the p24-containing gag precursor, p55. They also observed that a recombinant p24 formed an anti-p24 immunoreactive material. This indicated the occurrence of alterations of p24, and such alterations may be able to inhibit the release of reverse transcriptase activity....
...Regarding other viruses, a noteworthy finding is that hypericin completely inactivated bovine diarrhea virus (BVDV) in vitro in the presence of light (Prince et al. 2000)....
11.6.3. Anticancer Properties
Hyperforin and hypericin have also been examined for their anticancer properties. According to Schempp et al. (2002), hyperforin inhibits tumor cell growth in vitro. The mechanism involves induction of apoptosis (programmed cell death) through the activation of caspases, which are cysteine proteases that trigger a cascade of proteolytic cleavage occurrences in mammalian cells. Hyperforin also causes the release of cytochrome c from isolated mitochondria. Mitochondrial activation is an early event in hyperforin-mediated apoptosis, and hyperforin inhibits tumor growth in vivo (Schempp et al. 2002).
Schempp and his colleagues agreed that since hyperforin has significant antitumor activity, is readily available in high quantities (since it is naturally occurring in abundance), and has low toxicity in vivo, hyperforin holds promise of being an interesting novel antineoplastic agent. Other in vitro studies demonstrated that hyperforin in conjunction with polyphenolic procyanidin B2 effectively inhibited the growth of leukemia K562 and U937 cells, brain glioblastoma cells LN229, and normal human astrocytes (Hostanska et al. 2003).
Hypericin has also been investigated as an anticancer agent, reportedly inhibiting the growth of cells derived from a variety of neoplastic tissues, including glioma, neuroblastoma, adenoma, mesothelioma, melanoma, carcinoma, sarcoma, and leukemia (Fox et al. 1998).
The activity of hypericin is attributed to its photodynamic properties (Agostinis et al. 2002). In the presence of light and oxygen, hypericin acts as a powerful natural photosensitizer, generating superoxide radicals that form peroxide or hydroxyl radicals, or singlet oxygen molecules that kill tumor cells.
In this way, hypericin can be used as a component of photodynamic therapy (PDT; Agostinis et al. 2002). At first, PDT was used only for skin lesions, but it is becoming increasingly accepted as a treatment for many types of tumors.