Red Algae Extract Deters Ebola, HIV, SARS and HCV in Studies
While researchers scramble to develop a vaccine or monoclonal antibody against the Ebola virus – and continue to develop chemo treatments to stem HIV and Hepatitis-C while fearing SARS – nature has already provided a natural treatment.
Research has shown that a healthy strong immune system can allow a person to not only avoid contracting the disease – but become resistant to it as well. For those of us who need help or extract assurance, red algae proves to provide a key antiviral.
Hunting natural immunity for Ebola
After the two 1996 Ebola outbreaks in Gabon Africa, medical scientists determined that Ebola causes death among about 70 percent of those who contracted the virus.
This question led researchers from Gabon’s Franceville International Center of Medical Research to investigate. The questions ensued: Why don’t the other 30 percent die? How do 30 percent of those infected recover?
Furthermore, medical researchers found many instances where there were close contacts of those who became infected who never were infected at all. Even though they were in contact with the infected patient while the patient was symptomatic.
Note: An infected patient with Ebola must be symptomatic in order to be contagious – with fever and other flu-like symptoms. A person must also have direct contact with body fluids of an infected person in order to become infected with the virus. This means contact with saliva, urine, semen or blood – which can include contact with needles or other contaminated objects.
Thus, when the researchers investigated “close contact” individuals, they focused upon those who had this sort of exposure.
The research found that nearly half of those who were asymptomatic and seemingly immune developed antibodies (IgM and IgG) to the Ebola virus. This means these individuals certainly were intimately exposed to the virus, but simply naturally developed the immunity tools – including those discussed below – that prevented the infection from replicating out of control.
Furthermore, the asymptomatic group exhibited greater inflammatory responses in general. They were found to have higher levels of circulating cytokines and chemokines – which speed up the body’s natural ability to break down the viral cells and stop their activity within the body. They concluded:
“Asymptomatic individuals had a strong inflammatory response characterised by high circulating concentrations of cytokines and chemokines.”
Mannose-binding lectins attack Ebola virus
The particular mechanism with which the body naturally breaks down and prevents infection from lethal infections including Ebola, HIV, HCV, and SARS has gradually emerged. The mechanism is called mannose-binding lectins.
Mannose-binding lectins are apparently produced in the human body via a DNA sequence, called the MBL2. When this part of our genes is in order, the body will produce and release these mannose-binding lectins into the bloodstream.
Mannose-binding lectins will then recognize and glom onto certain carbohydrate molecules that cover and make up various microorganisms. These include fungi, bacteria, and even parasites, which utilize glycoprotein shells to protect themselves. But they also include viruses.
Once the lectins attach to these shells, they will break apart the surface of the microbe and basically break it down, allowing the body’s other immune cells to kill off the microbe and prevent it from replicating.
In fact, a healthy body that produces good levels of these mannose-binding lectins will be able to easily fight off colds and flu, as well as other microbial infections. Several animal studies have shown mannose-binding lectins heartily beat down coronaviruses and infectious bronchitis.
Research over the past five years has found that low levels of mannose-binding lectins increase the risk of respiratory infections, including syncytial virus infections, pneumonia, and others.
For example, in a study of 121 children, RSV-infections were associated with low levels of mannose-binding lectins. Nearly 70 percent of RSV-infected children had low levels of mannose-binding lectins.
But other infections – especially those related to bacterial infections – are not necessarily connected with mannose-binding lectin levels.
When it comes to virulent infections such as Ebola, Hepatitis C and HIV, however, these are different. These viruses come with glycoprotein shells that protect the virus from being broken down.
Furthermore, the glycoprotein shell of the Ebola virus produces glycoproteins that damage cells, allowing the virus to penetrate and replicate within the cell.
Mannose-binding lectins actually break down this shell and the glycoprotein matrix through a mechanism called the lectin pathway.
Humans that don’t produce enough of these mannose-binding lectins are not only more susceptible because they don’t have enough lectins, but they are typically also immunosuppressed with regard to the rest of their immune system.
One of the reasons some humans don’t produce enough mannose-binding lectins is because of a slight genetic mutation, where the MBL2 gene is switched off. The reason for this mutation/switch-off has yet to be fully understood. (Guess – something to do with our toxic environment and/or nutritional deficiency.)
Mannose-binding lectins from Red Algae
This brings us to the fun part. Yes, humans aren’t the only critters that produce mannose-binding lectins. Red algae also produce these profusely, which allow the algae to protect themselves from invasion by viruses.
The most promising form of mannose-binding lectins is a component of the Scytonema varium red algae called Scytovirin. The protein extract was isolated by researchers from the National Cancer Institute at Frederick, Maryland in 2003. The protein contains 95 amino acids, and was found to bind to HIV-1 viral shells.
A similar antiviral protein was found in Nostoc ellipsosporum – called Cyanovirin-N. Both of these antiviral proteins did similar things – they broke down the glycoprotein shells of HIV and HCV.
Yet another anti-viral extract was found from the New Zealand red alga species, Griffithsia sp. This protein is called Griffithsin, abbreviated with GRFT.
Over the next few years, Griffithsin was tested against HIV-1 with great success in laboratory studies, which included studies with mice. The epidemic-potential virus SARS was also tested against Griffithsin, also with great success.
Multiple studies illustrated these effects. Research from the Center for Cancer Research in Frederick, Maryland found that Griffithsin not only stopped HIV-1 virus replication, but stopped cellular intrusion of the virus.
In 2010 Harvard researchers tested a recombinant version of Griffithsin – called rhMBL – against Ebola. Once again, they found the mannose-binding lectins were able to not only breakdown the viral shells of the Ebola, but when given to mice infected with Ebola, the mice became immune to the virus.
Yes, when the mice given the recombinant mannose-binding lectins were rechallenged with the Ebola virus, they were found to be immune to the virus.
Since that study other research has tested other animals with Griffithsin, with similar results.
Any doubts about the seriousness of Griffithsin’s ability to treat Ebola should be squelched by the reality that the Griffithsin compound has been patented by the government of the United States, specifically for its ability to treat Ebola, SARS, hepatitis C and H5N1 virus.
On December 1, 2006, the patent was filed and granted – U.S. Patent #US 8088729 B2.
The interesting thing here is that the inventors of the patent are listed as: Barry O’Keefe, Toshiyuki Mori, James B. McMahon – the researchers who had been testing Griffithsin isolated from red marine algae.
But the shocker here is that the Original Assignee of the patent – the assigned owner of the patent is:
“The United States Of America As Represented By The Secretary, Department Of Health And Human Services”
In the “Claims” section of the patent we find the following:
“1. A method of inhibiting a viral infection of a host comprising administering to the host an anti-viral polypeptide comprising SEQ ID NO: 3, wherein the viral infection is a Hepatitis C viral infection, a Severe Acute Respiratory Syndrome (SARS) viral infection, an H5N1 viral infection, or an Ebola viral infection, and whereupon the viral infection is inhibited.”
The patent also states:
“An initial observation, which led to the invention, was anti-viral activity of certain extracts from a marine organism, namely Rhodophyte (Griffithsia sp.), originally collected in the territorial waters of New Zealand. Low picomolar concentrations of a protein isolated from the extracts, referred to herein as Griffithsin, irreversibly inactivated human clinical isolates of HIV. Its HIV molecular target is high mannose-comprised oligosaccharide constituents of Env glycoproteins. Upon binding, Griffithsin inhibits viral binding, fusion, and entry. Griffithsin also targets other viruses, such as other retroviruses, e.g., EV, SIV and HTLV, and non-retroviruses, such as measles and, especially, influenza (e.g., H5N1 virus), Ebola, Hepatitis C, and SARS virus.”
The question this of course brings up is quite clear: Why would the United States and the Department Of Health And Human Services quietly file a patent on a treatment for Ebola, HIV, SARS and Hepatitis-C? You tell me.
Recombinant Griffithsin produced in Nicotiana benthamiana plants
As modern medical researchers continually strive for isolated and synthesized versions of nature able to be patented, recombinant versions of Griffithsin were eventually produced using Nicotiana benthamiana plants (a relative of the tobacco plant). These plants were genetically modified so they would produce the same mannose-binding lectins.
This form of Griffithsin was tested on mice and guinea pigs infected with HIV-1, with successful antiviral results.
This was also found when testing the recombinant Griffithsin on Ebola-infected mice.
In all the studies, the Griffithsin was found to be safe and tolerated.
As to whether red algae can be taken in natural form to increase immunity, there is no doubt this is the case. Prior to this antiviral research that has spiraled into biopharm research, red algae had been shown to have antiviral and anticancer effects.
So the most logical answer is “yes” – certainly consuming red algae in supplement form has been found to boost antiviral immunity, and from the available research, blood levels of mannose-binding lectins. This should in turn boost immunity and create a natural method of preventing and even treating viral infections such as Ebola, SARS, HIV and Hepatitis-C.
This strategy should of course be used with a general immunity-boosting lifestyle.
Other plants also produce these mannose-binding lectins, some of which have been used in traditional medicines. A study from Belgium’s University of Leuven studied 33 different plant lectins, and found 10 different mannose-binding lectins among the plants that inhibited coronovirus, and intervened upon the replication cycle of SARS-CoV.
Consult with your health professional if you are sick.
Baize S, Leroy EM, Georges-Courbot MC, Capron M, Lansoud-Soukate J, Debré P, Fisher-Hoch SP, McCormick JB, Georges AJ. Defective humoral responses and extensive intravascular apoptosis are associated with fatal outcome in Ebola virus-infected patients. Nat Med. 1999 Apr;5(4):423-6.
Leroy EM, Baize S, Volchkov VE, Fisher-Hoch SP, Georges-Courbot MC, Lansoud-Soukate J, Capron M, Debré P, McCormick JB, Georges AJ. Human asymptomatic Ebola infection and strong inflammatory response. Lancet. 2000 Jun 24;355(9222):2210-5.
Albert RK, Connett J, Curtis JL, Martinez FJ, Han MK, Lazarus SC, Woodruff PG. Mannose-binding lectin deficiency and acute exacerbations of chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2012;7:767-77. doi: 10.2147/COPD.S33714.
Ribeiro LZ, Tripp RA, Rossi LM, Palma PV, Yokosawa J, Mantese OC, Oliveira TF, Nepomuceno LL, Queiróz DA. Serum mannose-binding lectin levels are linked with respiratory syncytial virus (RSV) disease. J Clin Immunol. 2008 Mar;28(2):166-73.
Barton C, Kouokam JC, Lasnik AB, Foreman O, Cambon A, Brock G, Montefiori DC, Vojdani F, McCormick AA, O’Keefe BR, Palmer KE. Activity of and effect of subcutaneous treatment with the broad-spectrum antiviral lectin griffithsin in two laboratory rodent models. Antimicrob Agents Chemother. 2014;58(1):120-7. doi: 10.1128/AAC.01407-13.
Takebe Y, Saucedo CJ, Lund G, Uenishi R, Hase S, Tsuchiura T, Kneteman N, Ramessar K, Tyrrell DL, Shirakura M, Wakita T, McMahon JB, O’Keefe BR. Antiviral lectins from red and blue-green algae show potent in vitro and in vivo activity against hepatitis C virus. PLoS One. 2013 May 21;8(5):e64449. doi: 10.1371/journal.pone.0064449.
Mori T, O’Keefe BR, Sowder RC 2nd, Bringans S, Gardella R, Berg S, Cochran P, Turpin JA, Buckheit RW Jr, McMahon JB, Boyd MR. Isolation and characterization of griffithsin, a novel HIV-inactivating protein, from the red alga Griffithsia sp. J Biol Chem. 2005 Mar 11;280(10):9345-53.
Bokesch HR, O’Keefe BR, McKee TC, Pannell LK, Patterson GM, Gardella RS, Sowder RC 2nd, Turpin J, Watson K, Buckheit RW Jr, Boyd MR. A potent novel anti-HIV protein from the cultured cyanobacterium Scytonema varium. Biochemistry. 2003 Mar 11;42(9):2578-84.
Michelow IC, Lear C, Scully C, Prugar LI, Longley CB, Yantosca LM, Ji X, Karpel M, Brudner M, Takahashi K, Spear GT, Ezekowitz RA, Schmidt EV, Olinger GG. High-dose mannose-binding lectin therapy for Ebola virus infection. J Infect Dis. 2011 Jan 15;203(2):175-9. doi: 10.1093/infdis/jiq025.
Vorup-Jensen T, Sørensen ES, Jensen UB, Schwaeble W, Kawasaki T, Ma Y, Uemura K, Wakamiya N, Suzuki Y, Jensen TG, Takahashi K, Ezekowitz RA, Thiel S, Jensenius JC. Recombinant expression of human mannan-binding lectin. Int Immunopharmacol. 2001 Apr;1(4):677-87.
Singh RS, Thakur SR, Bansal P. Algal lectins as promising biomolecules for biomedical research. Crit Rev Microbiol. 2013 Jul 16.
Keyaerts E, Vijgen L, Pannecouque C, Van Damme E, Peumans W, Egberink H, Balzarini J, Van Ranst M. Plant lectins are potent inhibitors of coronaviruses by interfering with two targets in the viral replication cycle. Antiviral Res. 2007 Sep;75(3):179-87.