O.k. first what do we know about epidemics or pandemics? We know that air born virus' spread very quickly. The H1N1 took 7 months to go world wide. We know that in the case of HIV it took between 60 and 70 years for it to become a pandemic. (Basically 1915 to 1975/85.)
HIV is spread both through sexual contact, and passed via blood from mother to child or in the case of transfusions. It's estimated that it took around 10 to 20 people being infected with SIV originaly in order for the virus to mutate and effectively infect humans hence it became HIV.
The human HIV infection is traced to bush hunters along the African coast who hunted and killed monkey's for meat to sell. By butchering the monkeys into meat they came in contact with large quantities of blood. These individuals were usually single men who often made stops in ports or cities to sell the meat. They passed the HIV on to whomever they had intercourse with. And those individuals passed it on and so on and so on. Most of these individuals were sexually active with multiple partners and so were able to keep the virus alive by passing it on before becoming sick and dying.
So using that information how can we extrapolate the spread of XMRV with high rates of cases showing up in the 1980's? Well what do we know about XMRV to date?
We know for a fact that XMRV is transmittable in male semen as noted in the study
Fibrils of Prostatic Acid Phosphatase Fragments Boost Infections with XMRV (Xenotropic Murine Leukemia Virus-Related Virus), a Human Retrovirus Associated with Prostate Cancer Received 6 February 2009/ Accepted 21 April 2009 by the journal of Virology
The study states ;
1. Furthermore, XMRV RNA was detected in prostatic secretions of some men with prostate cancer. The fact that the precursor of SEVI is produced in abundance by the prostate indicates that XMRV replication occurs in an environment that provides a natural enhancer of viral infection, and this may play a role in the spread of this virus in the human population.
We don't know if it is spread via vaginal fluids at this time since a study has not been done on this but I would think it a pretty good bet that it does.
We know for certain that it spreads via blood and blood sera or plasma based on
Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome
The study states
We next investigated whether the viral proteins detected in PBMCs from CFS patients represent infectious XMRV. Activated lymphocytes. . . as well as virus preparations from these cells (Fig. 3C), revealed 90- to 100-nm-diameter budding particles consistent with a gamma (type C) retrovirus.
We also found that XMRV could be transmitted from CFS patient plasma to LNCaP cells when we applied a virus centrifugation protocol to enhance infectivity (6, 14, 15). Both XMRV gp70 Env and p30 Gag were abundantly expressed in LNCaP cells incubated with plasma samples from 10 of 12 CFS patients, whereas no viral protein expression was detected in LNCaP cells incubated with plasma samples from 12 healthy donors (Fig. 4A). Likewise, LNCaP cells incubated with patient plasma tested positive for XMRV p30 Gag in IFC assays (fig. S5B). We also observed cell-free transmission of XMRV from the PBMCs of CFS patients to the T cell line SupT1 (Fig. 4B) and both primary and secondary
transmission of cell-free virus from the activated T cells of CFS patients to normal T cell cultures (Fig. 4C). Together, these results suggest that both cell-associated and cell-free transmission of CFS-associated XMRV are possible.
We don't know if XMRV is spread via saliva since no study has been done on this. HIV is not transmissible through saliva or casual contact so most likely the XMRV retrovirus won't be either. And while we do know that it is present in the respiratory tract (so is HIV) we don't know if it is transmissible this way. If it's like HTLV-1/2 and HIV-1/2 then it won't be airborn. Plus based on the total number of cases currently 17 million ill and over 180 million infected it would have to have become airborn in the early 2000's (look at the spread of H1N1) And we know that it goes back to at least 1934 and possibly to 1850.
Base on the information coming from the founding fathers and mothers of this retrovirus we are hearing that a cofactor is needed to activate the XMRV into an participant in XAND related illnesses. (CFS/ME, autism, atypical MS, cancer, and possibly others) So each of us had to have had the XMRV retrovirus before we were hit by another virus say EBV which activated the XMRV.
The way I understand it the activating virus is stimulated the immune system thus providing host T,B, and NK cells. XMRV likes those cell especially for replication. So EBV or which ever virus provided the opportunity for the XMRV to replicate. That replication process is why those infected never got better.
Most of us are familiar with the X graph.
My speculation is that when you are hit by a normal everyday virus that would normally not be a problem for you to deal with, what is actually happening is that you are creating homes for XMRV to move into and raise some kids. And they never leave.
If the HIV pandemic took around 60 to 70 years to infect enough people to become noticeable in the general population then it's not too much of a stretch to figure that the same rate might apply to XMRV. The XMRV became noticeable in the 1980 and was still noticeable in the 1990's. Meaning by the 1980's a good portion of the population had the virus. So if you are sharing the flu bug in your office then it would stand to reason that a number of individuals in your office would come down with a XAND illness sometimes known as CFS.
Right now there are possibly 10 million American walking around with XMRV just waiting for the right event to trigger them. My guess is that some of those people will never come down with anything. Some may have stronger immune systems, the right set of genetics to fight it off or perhaps less of a viral load. These are the dark areas that need the light of many studies to say for sure.
The next question of how did we all become infected and why were their so many outbreaks in the 80's. I have a theory on that and it's just theory but try it out and see if it fits. Most of the PhD people start the outbreaks in 1934 at Los Angeles General Hospital. I've seen some theory's that go back to 1850 but most start with 1934 and work their way forward.
Remember that it was between 1975 and 1985 that the HIV pandemic peaked approximately 60 to 70 years after the initial jump of SIV to human HIV. Which puts the initial infections of HIV to somewhere between 1890 and 1915. Now if XMRV followed something like the same path and we look between 60 to 70 years from the peak outbreak years you are look around 1915 to 1930 for an event that would allow for XMRV a variant of MLV or mouse virus to enter the human population undetected and be passed on and on an on. So what was that event?
I found a good article here that may explain how the jump in species occurred.
I'll quote from the article
It all starts in 1900 with Abbie E.C. Lathrop of Granby, Mass. Lathrop was a 32-year-old former schoolteacher who had moved to Granby around that time with the notion of starting a poultry farm. That soon flopped, and she switched from chickens to rodents, hoping to cash in on the Victorian craze for "fancy" mice.
At around the same time a Harvard University zoologist named William Castle ordered mice to begin working on genetic experiments. He was a leader in his field at the time. However the man who would ultimately solidify the mouse as perfect for genetic and laboratory testing was one of Castle's undergraduate students, Clarence Cook Little.
Little's innovation was the "inbred strain." By mating brother to sister over and over, he created rodents that were genetically alike. In fact, after 20 generations the mice were nearly 99 percent identical. In 1909 he created the first inbred strain, dba, which is still used in research. Before inbred strains, scientists couldn't say for certain whether their results were because of the genetic quirks of a particular mouse or the experiments.
Is it possible then that one or more of these "inbred strains" carried a mutated form of MLV which would remain unnamed for a century? I don't know for a fact that this is the case however I do know that these mice where shipped to hundreds of laboratories and research facilities around the US and world. by 1929 bigger and better mouse holding facilities were needed. Little persuaded auto industry tycoons Edsel Ford (son of Henry) and Roscoe Jackson, chief of Hudson Motorcar Co., to finance an independent research facility, Jackson Laboratory, near one of their favorite vacation spots, Bar Harbor, Maine. Mouse research bloomed. Pasted from <http://pages.slc.edu/~krader/sunarticle.html>
Now the first outbreak is usually figured as the Los Angeles County General Hospital so let's look at that.
In 1896 USC medical school and teaching facility opened it closed from lack of funds in 1910 and reopened in 1928. It was affiliated with Los Angeles County General Hospital which opened a new modern county hospital on State Street in 1933 in what is today the Los Angeles County and USC Medical Center.
So the theory would go like this. . .
Much like the HIV infection of bush hunters, XMRV infected between 10 and 20 persons in the Los Angeles county hospital by way of the USC teaching and research facility and probably many more persons. The XMRV retrovirus lays dormant in the population being passed on and on, including future generations of children. Until, it is activated by a Co-infection. Hence the 1934 outbreak at L.A. General. Since then hundreds of thousands of people have become infected around the world we now have a pandemic. Manifesting in a variety of ways based on genetic predisposition.
My family is from LA originally and both my mother and I were born at L.A. General hospital. My mother had uterine cancer at age 28. She was diagnosed with Major Depressive Disorder in her 30's. She came down with lymphoma at 39 and died at age 47 in 1991.
Me I've enjoyed perfect health all my life. Hiking, Biking and generally enjoying all that life has to offer. When I decided to go into teaching at age 36 that's when I started getting sick. Every time I got the "illness of the year" that was going around, Mono or flu or what ever I became a little weaker until finally I got sick and didn't recover at all.
So anyway that's my Outbreak theory. Colonel Mustard in the Library with a candle stick!!!
HIV is spread both through sexual contact, and passed via blood from mother to child or in the case of transfusions. It's estimated that it took around 10 to 20 people being infected with SIV originaly in order for the virus to mutate and effectively infect humans hence it became HIV.
The human HIV infection is traced to bush hunters along the African coast who hunted and killed monkey's for meat to sell. By butchering the monkeys into meat they came in contact with large quantities of blood. These individuals were usually single men who often made stops in ports or cities to sell the meat. They passed the HIV on to whomever they had intercourse with. And those individuals passed it on and so on and so on. Most of these individuals were sexually active with multiple partners and so were able to keep the virus alive by passing it on before becoming sick and dying.
So using that information how can we extrapolate the spread of XMRV with high rates of cases showing up in the 1980's? Well what do we know about XMRV to date?
We know for a fact that XMRV is transmittable in male semen as noted in the study
Fibrils of Prostatic Acid Phosphatase Fragments Boost Infections with XMRV (Xenotropic Murine Leukemia Virus-Related Virus), a Human Retrovirus Associated with Prostate Cancer Received 6 February 2009/ Accepted 21 April 2009 by the journal of Virology
The study states ;
1. Furthermore, XMRV RNA was detected in prostatic secretions of some men with prostate cancer. The fact that the precursor of SEVI is produced in abundance by the prostate indicates that XMRV replication occurs in an environment that provides a natural enhancer of viral infection, and this may play a role in the spread of this virus in the human population.
We don't know if it is spread via vaginal fluids at this time since a study has not been done on this but I would think it a pretty good bet that it does.
We know for certain that it spreads via blood and blood sera or plasma based on
Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome
The study states
We next investigated whether the viral proteins detected in PBMCs from CFS patients represent infectious XMRV. Activated lymphocytes. . . as well as virus preparations from these cells (Fig. 3C), revealed 90- to 100-nm-diameter budding particles consistent with a gamma (type C) retrovirus.
We also found that XMRV could be transmitted from CFS patient plasma to LNCaP cells when we applied a virus centrifugation protocol to enhance infectivity (6, 14, 15). Both XMRV gp70 Env and p30 Gag were abundantly expressed in LNCaP cells incubated with plasma samples from 10 of 12 CFS patients, whereas no viral protein expression was detected in LNCaP cells incubated with plasma samples from 12 healthy donors (Fig. 4A). Likewise, LNCaP cells incubated with patient plasma tested positive for XMRV p30 Gag in IFC assays (fig. S5B). We also observed cell-free transmission of XMRV from the PBMCs of CFS patients to the T cell line SupT1 (Fig. 4B) and both primary and secondary
transmission of cell-free virus from the activated T cells of CFS patients to normal T cell cultures (Fig. 4C). Together, these results suggest that both cell-associated and cell-free transmission of CFS-associated XMRV are possible.
We don't know if XMRV is spread via saliva since no study has been done on this. HIV is not transmissible through saliva or casual contact so most likely the XMRV retrovirus won't be either. And while we do know that it is present in the respiratory tract (so is HIV) we don't know if it is transmissible this way. If it's like HTLV-1/2 and HIV-1/2 then it won't be airborn. Plus based on the total number of cases currently 17 million ill and over 180 million infected it would have to have become airborn in the early 2000's (look at the spread of H1N1) And we know that it goes back to at least 1934 and possibly to 1850.
Base on the information coming from the founding fathers and mothers of this retrovirus we are hearing that a cofactor is needed to activate the XMRV into an participant in XAND related illnesses. (CFS/ME, autism, atypical MS, cancer, and possibly others) So each of us had to have had the XMRV retrovirus before we were hit by another virus say EBV which activated the XMRV.
The way I understand it the activating virus is stimulated the immune system thus providing host T,B, and NK cells. XMRV likes those cell especially for replication. So EBV or which ever virus provided the opportunity for the XMRV to replicate. That replication process is why those infected never got better.
Most of us are familiar with the X graph.
My speculation is that when you are hit by a normal everyday virus that would normally not be a problem for you to deal with, what is actually happening is that you are creating homes for XMRV to move into and raise some kids. And they never leave.
If the HIV pandemic took around 60 to 70 years to infect enough people to become noticeable in the general population then it's not too much of a stretch to figure that the same rate might apply to XMRV. The XMRV became noticeable in the 1980 and was still noticeable in the 1990's. Meaning by the 1980's a good portion of the population had the virus. So if you are sharing the flu bug in your office then it would stand to reason that a number of individuals in your office would come down with a XAND illness sometimes known as CFS.
Right now there are possibly 10 million American walking around with XMRV just waiting for the right event to trigger them. My guess is that some of those people will never come down with anything. Some may have stronger immune systems, the right set of genetics to fight it off or perhaps less of a viral load. These are the dark areas that need the light of many studies to say for sure.
The next question of how did we all become infected and why were their so many outbreaks in the 80's. I have a theory on that and it's just theory but try it out and see if it fits. Most of the PhD people start the outbreaks in 1934 at Los Angeles General Hospital. I've seen some theory's that go back to 1850 but most start with 1934 and work their way forward.
Remember that it was between 1975 and 1985 that the HIV pandemic peaked approximately 60 to 70 years after the initial jump of SIV to human HIV. Which puts the initial infections of HIV to somewhere between 1890 and 1915. Now if XMRV followed something like the same path and we look between 60 to 70 years from the peak outbreak years you are look around 1915 to 1930 for an event that would allow for XMRV a variant of MLV or mouse virus to enter the human population undetected and be passed on and on an on. So what was that event?
I found a good article here that may explain how the jump in species occurred.
I'll quote from the article
It all starts in 1900 with Abbie E.C. Lathrop of Granby, Mass. Lathrop was a 32-year-old former schoolteacher who had moved to Granby around that time with the notion of starting a poultry farm. That soon flopped, and she switched from chickens to rodents, hoping to cash in on the Victorian craze for "fancy" mice.
At around the same time a Harvard University zoologist named William Castle ordered mice to begin working on genetic experiments. He was a leader in his field at the time. However the man who would ultimately solidify the mouse as perfect for genetic and laboratory testing was one of Castle's undergraduate students, Clarence Cook Little.
Little's innovation was the "inbred strain." By mating brother to sister over and over, he created rodents that were genetically alike. In fact, after 20 generations the mice were nearly 99 percent identical. In 1909 he created the first inbred strain, dba, which is still used in research. Before inbred strains, scientists couldn't say for certain whether their results were because of the genetic quirks of a particular mouse or the experiments.
Is it possible then that one or more of these "inbred strains" carried a mutated form of MLV which would remain unnamed for a century? I don't know for a fact that this is the case however I do know that these mice where shipped to hundreds of laboratories and research facilities around the US and world. by 1929 bigger and better mouse holding facilities were needed. Little persuaded auto industry tycoons Edsel Ford (son of Henry) and Roscoe Jackson, chief of Hudson Motorcar Co., to finance an independent research facility, Jackson Laboratory, near one of their favorite vacation spots, Bar Harbor, Maine. Mouse research bloomed. Pasted from <http://pages.slc.edu/~krader/sunarticle.html>
Now the first outbreak is usually figured as the Los Angeles County General Hospital so let's look at that.
In 1896 USC medical school and teaching facility opened it closed from lack of funds in 1910 and reopened in 1928. It was affiliated with Los Angeles County General Hospital which opened a new modern county hospital on State Street in 1933 in what is today the Los Angeles County and USC Medical Center.
So the theory would go like this. . .
Much like the HIV infection of bush hunters, XMRV infected between 10 and 20 persons in the Los Angeles county hospital by way of the USC teaching and research facility and probably many more persons. The XMRV retrovirus lays dormant in the population being passed on and on, including future generations of children. Until, it is activated by a Co-infection. Hence the 1934 outbreak at L.A. General. Since then hundreds of thousands of people have become infected around the world we now have a pandemic. Manifesting in a variety of ways based on genetic predisposition.
My family is from LA originally and both my mother and I were born at L.A. General hospital. My mother had uterine cancer at age 28. She was diagnosed with Major Depressive Disorder in her 30's. She came down with lymphoma at 39 and died at age 47 in 1991.
Me I've enjoyed perfect health all my life. Hiking, Biking and generally enjoying all that life has to offer. When I decided to go into teaching at age 36 that's when I started getting sick. Every time I got the "illness of the year" that was going around, Mono or flu or what ever I became a little weaker until finally I got sick and didn't recover at all.
So anyway that's my Outbreak theory. Colonel Mustard in the Library with a candle stick!!!
