HIV and herbal medicine; the use of St Johns Wort and Panax ginseng.

by Hananja Brice-Ytsma Medical Herbalist (MSc, MNIMH)

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HIV and herbal medicine

The introduction of highly active antiretrovital therapy (HAART) into clinical

practice has dramatically changed the development of HIV-related diseases in
industrialised countries (Vella 2000) but HIV infection still remains an incurable
disease (Wei et al 1995). HAART alone cannot eradicate the virus in the human body
(Finzi et al). Drug resistance is probably the most important factor contributing
to the failure of treatment today (Richman D 1997). The antiretrovirals have an
impact on reducing morbidity and mortality, prolonging lives, improving the
quality of life of many people living with HIV (WHO 2002). Many people in
developing countries cannot afford the high cost of HAART (Asres et al 2005), it
has a limited response in some patients, it has a complicated dosage regimen
leading to non-compliance, and is associated with drug toxicity and the emergence
of drug resistance (Bonfanti et al 1999). The majority of people living with HIV
are using complementary medicine (Ozsoy 1999). In Europe herbal treatments have
been the most popular complementary medicine used by HIV infected individuals
(Ozsoy 1999). Research has been carried out and is in progress to isolate the
active constituents from plants for the prevention of transmission of HIV and
treatment of AIDS (Asres et all 2005). Many plants are active against HIV
replication at least in vitro, whose significance is not yet clear, and have not
been followed up to see their actual clinical usefulness in combating HIV/AIDS(De
Clercq 2000). Being a relatively new disease there is no tradition of herbs used
for HIV/AIDS. So is there any clinical evidence for use of herbal medicine in HIV
positive patients?

Panax ginseng (Korean Red Ginseng KRG)

Panax ginseng is an herbal root that has been known in China for more than 2000
years (Li et al 1973). A study in healthy human volunteers revealed that KRG
significantly increases neutrophil, CD4 T cells and NK cell function (Scallione et
al 1990). Ginseng was found to increase the cellular immune functions of
peripheral blood mononuclear (PBMC) from AIDS patients and normal individuals (See
et al 1997). KRG was given for 6 months to HIV-1 infected individuals (5.4mg
daily), CD4T cell counts in HIV-1-infected patients treated with only KRG were
maintained or even increased for a prolonged period. The development of resistance
mutations in RT to zidovudine (ZDV) was delayed by combined therapy with KRG and
ZDV (Cho et al 1993). Some of those patients have maintained CD4+ count for 8
years with KRG-intake only (Cho et al 2001). It was suggested that the maintenance
of CD4T cell counts by ZDV and KRG intake for a prolonged period might be
indirectly associated with delayed development of resistance to ZDV by KRG intake
(Cho et al 2001). No details are given on the trial itself, the number of patients
involved, the stage of disease, no control, so we cannot draw any conclusion of
the above but the initial observation led to the following study done by the same
authors. A study investigated whether the maintenance of CD4+ T cell count in HIV-
1-infected patients treated with ZDV and KRG is associated with the delay of the
development of resistance to ZDV (Cho et al 2001). Nine of the 18 pt were in the
KRG group, daily dose of 5.4g, and had been treated with KRG for 60 months and ZDV
for more than 18 months, nine were in the control group and been treated with ZDV
only. KRG intake was the only significant variable between the two groups. There
was no significant difference in clinical stages and demographics between the KRG
group and the control group. Maintenance or increase in CD4+ T cell counts in
patients treated with KRG was found. Mild but consistent decrease in p24 antigen
during KRG-intake was also detected as long as KRG was taken. In Combination with
ZDV, the beneficial effects associated with KRG-intake were a decrease in CD4+ T
cell count was not detected during at least a few years of therapy. Based on these
observations, the authors concluded that KRG intake itself is likely to have
beneficial effects in HIV patients. Over the 24 months of treatment, the overall
incidence of 6 resistance mutations to ZDV was significantly reduced in the KRG
group. The authors conclude that the maintenance of CD4+ T cell counts by ZDV and
KRG-intake for a prolonged period might be indirectly associated with delayed
development of resistance to ZDV by KRG-intake. The authors recommend KRG intake
as early stage as possible to get good prognosis over a long term. The number in
this study is very small but well accounted for. There was a significant time
scale used. Individuals respond different to the virus and cofactors could lead to
earlier development of AIDS. Being such a small number it is difficult to say how
valid and reliable the measurements were. The patients and investigators were not
blinded. No side effects were reported. The data suggests that the combination of
antiretroviral drugs with KRG could be a new therapeutic modality to treat HIV-1
infected patients but larger trials are needed. KRG was tested with ZDV so we
cannot draw a conclusion on the combination of other antiretroviral drugs with KRG
and that would need to be investigated.

Another original study was done to investigate whether this slow progression or
maintenance of CD4 T cell over 10 years was affected by KRG intake alone or in
combination with HLA factor (Sung et al 2004). Many patients have maintained their
CD4 T cell counts for more than 10 years without antiretroviral drugs therapy and
prognosis of HIV-1 infected patients has been found to be strongly associated with
their HLA alleles. They determined HLA class I in 90 HIV-1 infected patients
diagnosed from 1987 to 2001. They were randomly recruited nation-wide however, it
is not stated how. At enrolment the patients were asked to return for an interview
and for clinical examination and a blood sample every 6 months. Estimating the
rate of progression of HIV-1 infection was accomplished by measuring the annual
decrease in CD4 T cells. The HLA results were compared with those of a control
group, which was comprised of 199 uninfected Korean people drawn for the
population. 22 patients were treated with antiretroviral drugs or were monitored
for less than 60 months. Changes in the CD4 T cells and correlation among KRG
intake, CD4-Tcells and HLA were finally analysed in the 68 out of 90 patients. The
median follow up time in the 68 pt was 113.5 months (range 60-164 months. 61 out
of the 68 pt were treated with KRG (5.4g per day). A strong correlation was found
between KRG intake and annual decrease in CD4 T cells, and between KRG intake and
sCD8, together with a significant inverse correlation between HLA prognostic score
and annual decrease in CD4 cells. In addition they found that KRG intake alone
slows the decrease in CD4 T cells irrespective of HLA prognostic score. Also, a
significant decrease in serum sCD8 was found which is an immune activation marker
physiologically secreted from CD8T cells. The significant and consistent decrease
in serum sCD8 was maintained as long as KRG was taken continuously. Thus the
decrease in serum sCD8 may be indicative of a lower level of destruction of CD8 T
cells in patients ingesting KRG and suggests that KRG intake is associated with
prolonged maintenance of enhanced CD8T lymphocyte activity. The authors concluded
that KRG intake independently has beneficial effects on the slow decrease in CD4 T
cells and on serum sCD8 levels in HIV- infected patients, although the HLA factor
was also significantly associated with the rate of CD4 T cell depletion in the
Korean population.
The population studied was small, and only seven were not taking KRG, but over a
significant amount of time, no side effects are mentioned, patients and
investigators were not blinded so open to systematic bias. To say if the
measurements were valid, reliable, and reproducible, one might need a larger
group. The paper could point to possible use of KRG, but is difficult to conclude
without more rigorous trials.

Hypericum perforatum (HP); St John's Wort

Hypericum perforatum (HP); St John’s Wort

Hypericin or HP is taken commonly by HIV-infected persons (Kassler et al 1991).

Hypericin has activity against many HIV in vitro Hudson et al 1991). In 1989
researchers found that two extracts of HP had anti-HIV activity in lab experiments
with cells and viruses. Since hypericin is known to exhibit a similar inhibitory
property, it is likely to be one of the active constituents of St Johns wort
(Taher et al 2002). Hypericin appears to inactivate free virions and interfere
with steps in the replicative cycle (Hudson 1991). Hypericin and pseudohypericin
display an extremely effective antiviral activity when administered to mice after
retroviral infection (Muerelo et al 1988). It was found that relatively small
doses of hypericin or pseudohypericin 10-50ug per mouse can prolong survival of
HIV infected mice. When the compounds interact with the infection particles
shortly after in vivo administration, disease is completely prevented. The
compounds can cross the blood-brain barrier (Meruela et al 1988). Initial studies
looked promising (James 1989).

An uncontrolled study of 26 pt self-administering Hypericum containing herbal

extract (Cooper and James 1990) concomitant, used AZT, and other treatment was
permitted. All patients were HIV positive, at various stages of the disease, and
were taking approximately 1 mg total hypericin per day. They received baseline and
4 monthly checks, including physical examinations, T-cell subsets and p24 antigen.
Toxicity was limited to mild reversible liver enzyme elevation in 5 patients, with
levels returning to baseline after 1 month without Hypericum. At the end of the 4-
month study, p24 antigenaemia disappeared in 2 of 6 initially positive patients,
both also using AZT. CD4 cell changes differed, depending on AZT usage, in the
subgroup of 10 pt who had never taken AZT, none had developed AIDs, the mean CD4
count increased 13% from the base line after 1 month of Hypericum and maintained
this increase for 4 months. These increases were not statistically significant. By
contrast however, in those using Hypericum and AZT throughout the study, CD4
counts fell significantly after initial mild rise.
Details of the patients are minimal and there was no control group; size sample
was small and duration short. So, again, a study might not have any significance,
however this is the first pointer towards that hp might interfere with the
anitiviral AZT and as a consequence lower CD4 count.

A study was carried out to assess the toxicity and possible anti-HIV activity of
hypericin; there was no CD4 count criteria for entry (Fumer et al 1991). Four
different daily dosage levels of hypericin were administered (0.5mg, 2mg, 4mg,
8mg) to cohorts, often HIV-infected men, all HIV positive, no details of what
stage of disease, for a period of 12 weeks. No indication is given on the baseline
differences between the different groups. Possibly observed toxicities included
mild diarrhoea and indigestion, and infrequent itchy rash, and fatigue or
depression. An idiosyncratic, reversible elevation of hepatic transaminases was
also observed. No early, marked anti-HIV activity was found. The authors concluded
that at doses of 2mg per day given to HIV infected individuals, hypericin appears
to be safe for the majority of subjects observed so far (Moraleda et al 1993).
Duration of treatment was 12 weeks, which might be too short to notice any
beneficial effects. However the conclusion that 2 mg was a safe dose for the
majority of patients is important to look at.
An open clinical trial with (Steinbeck-Klose and Wernet 1993) 16 HIV patients at
various stages of the disease process were treated solely with Hypericum. No
statement on recruitment, inclusion or exclusion criteria, and no control group.
Standardised extract, 0.8mg total hypericin per week, plus 6 tablets of
unspecified strength. Patients showed stable or increasing counts of absolute CD4
values for helper T cells over the 40 months of observation. A significant length
of treatment compared to the other trial. This trend was not dependent on the
levels of the absolute CD4 count at the beginning of Hypericum treatment. Only 2
of the 16 encountered an opportunistic infection during the 40 months. The other
14 pt remained clinically stable and are active in work and life with a
karnoviski-index of 100 (a validated form of measurement). This correlated to the
stable values of haemoglobin, leukocytes and platelets. None of the known viral
complications due to cytomegalovirus, herpes or Epstein-Barr virus were
encountered. No side effects, including photosensitivity, were seen or measured in
any of the patients. With such as small study, and the many variables, one cannot
conclude any more than that it is of interest, and should be investigated in a
more rigorous study.

Hypericin can cause moderate to severe phototoxicity in people with HIV. In a

phase 1 trial (Gullick et al 1999), the researchers examined the safety and
antiviral activity of oral and intravenous hypericin in 30 HIV-positive patients
with fewer than 350 CD4+ cells/mm3. Subjects were excluded if they had significant
medical illnesses or were taking medication within 1 month of study entry. The
study was done in four clinical research units, open label, dose-escalation study
of intravenous or oral hypericin. 30 Patients enrolled in to three cohorts, that
received intravenous hypericin and one cohort that received oral hypericin. Groups
received 0.25 or 0.5mg/kg twice weekly or 0.25mg three times a week intravenously.
The oral dose of hypericin was 0.5mg/kg per day (n3). During the trial newly
observed toxic effects were observed and a scale for phototoxicity was
implemented. The drug used was synthesised by a pharmaceutical company, pure
hypericin. None finished the trial because of moderate or severe phototoxicity.
They concluded that 0.25mg/kg as the maximum tolerated dose for twice weekly
intravenous administration. The toxic reaction was an erythematous rash associated
with painful dysesthesias that involved areas exposed to light, consistent with a
cutaneous phototoxic reaction. This reaction resolved after discontinuation of
hypericin therapy. No clear evidence of antiretroviral activity was observed. The
authors concluded Hypericin therapy induced serious cutaneous phototoxicity and
lacked demonstrable antiretroviral activity at the doses tested in the study. They
also stated that these findings raised concerns about the safety of hypericin,
which is available as an herbal preparation and commonly used by HIV-infected
patients. They do however say that previous studies of hypericin and Hypericum in
both HIV-infected and non-HIV infected patients noted a relative lack of side
effects, although the doses were lower and the preparations were less pure than
those used in their study. In fact, the doses used are extremely high and near to
impossible to achieve when using the whole herb. Hypericin was synthesised by a
pharmaceutical company as opposed to coming from the plant itself, and when tried
on animals the herb was used. There might be other constituents in the plant
contributing to antiviral activity and this should be investigated. What has
become clear is that synthesised high doses of hypericin leads to severe
phototoxicity, and has no clear effect on the virus. Average doses of hypericin in
previous trials were between 1-2mg of hypericin per day. One or the above studies
concluded not to give more than 2 mg per day. The dose of hypericin described here
is much higher (5-10x).

Interaction with antivirals

St.John’s wort affects the activity of certain enzymes in the liver and intestines
that are used to process the following groups of HIV drugs (protease inhibitors
and non-nucleoside reverse transcriptase inhibitors), speeding the process up and
reducing the levels of these anti-HIV drugs to less than ideal levels (Piscitelli
et al 2000). In such situations, it is relatively easy for HIV to become resistant
to these drugs. Over time this can lead to increased levels of virus in the blood
and falling levels of immune system cells and, perhaps, life-threatening
infections. According to one study the use of HP can cause significant decrease in
indinavir levels in the blood, ranging from 49-99%, in addition to reducing the
efficacy of indinavir, such a large drop in the drug’s level may increase the risk
of resistance (Piscitelli et all 2000). Doctors have found that HP can reduce
levels of nevirapine a non-nuke nevirapine.

Conclusion

All the above studies are extremely small, and there was a loss of interest once
it became apparent that HP cannot be given together with antivirals. However there
might still be a role for HP when patients are not on antiviral. KRG could be of
benefit, but needs to be investigated with other antivirals. Outcome studies
examining the efficacy of herbal medicine among people living with HIV-AIDS are
often conducted among small sample sizes with very little follow-up data or time
points. It is difficult to conduct clinical studies in chronically ill patients
without participants dropping out, typically because studies’ demands, coupled
with their illness, become too burdensome. Small trials may cause random error for
both positive and negative findings, the treatment duration is not long enough for
endpoint outcomes such as mortality or new aids related events. Many studies with
small sample sizes reported trends, but did not find statistical significance.
Increasing sample sizes in further studies is necessary in order to evaluate the
scientific merit of these trends (Power et al 2002).
Future trials of herbal medicine should be large and should take into account the
clinical outcomes, such as progression to AIDS or AIDS-related illness and quality
of life, using longitudinal, controlled designs to accurately assess the safety of
such interventions (Power et al 2002).
Since studies have demonstrated the relationship between plasma HIV RNA loads, CD4
cell counts, and disease progression in HIV infection, these need to be included.
Compatibility and drugs interaction of any sort with conventional antiretrovirals
and other drugs commonly administered to AIDS patients should be studied. Many of
the anti-HIV natural products have other medicinal values; these types of
compounds may also be of interest as they can deal with both the virus and the
various disorders that characterise HIV/AIDS.

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