Archive for the ‘Viruses’ Category

Zoonotic Implications of Changing Tick Populations

October 25, 2018

Zoonotic Implications of Changing Tick Populations

As environmental changes allow tick populations to spread, the zoonotic risk of tickborne diseases increases.

By Kate Boatright, VMD

Between 1940 and 2004, the majority of emerging human infectious diseases worldwide were zoonotic. Of these, nearly one-quarter were arthropod vector-borne diseases, with ticks being the most common vector. In the United States, tickborne diseases account for about 95% of vector-borne diseases.

A recent review article in Veterinary Sciences examined many factors of tick biology, including the changing geographic distribution of tick populations and the impact of this change on associated tickborne diseases.

Ixodes Ticks and Associated Pathogens

Ixodid ticks exist worldwide. Warmer temperatures and changing humidity have allowed for northern expansion in North America, Europe, and Russia. Many significant zoonotic pathogens are carried by these ticks:

  • Borrelia burgdorferi, the causative agent of Lyme disease, is now seen throughout the United States, Canada, and Europe.
  • New Borrelia species identified worldwide have been implicated as additional causative agents of Lyme disease (Borrelia mayonii) and a relapsing fever (Borrelia miyamotoi).
  • Babesiosis, caused by over 100 different Babesia species, is especially significant for cattle and humans. Human babesiosis cases are expected to be seen in Canada due to the increased number of Ixodes scapularis ticks, and new Babesia species are now seen in regions not previously known to have babesiosis.
  • Anaplasma phagocytophilum is the causative agent of human granulocytic anaplasmosis (HGA), equine anaplasmosis, and febrile diseases in ruminants, cats, and dogs. Reports of HGA in the United States increased by a factor of 12 between 2001 and 2011.
  • Co-infections are common in individuals exhibiting disease from an Ixodes tick vector. Ten percent of individuals infected with Anaplasma also had antibodies to B burgdorferi or Babesia microti.
Ambylomma Ticks and Ehrlichia

In the United States, Amblyomma americanum ticks have expanded both north and west as white-tailed deer populations have increased in these regions. All life stages of this tick species can feed on humans and deer, increasing the potential for transmission of Ehrlichia chaffeensis and Ehrlichia ewingii, the most common causes of human monocytic ehrlichiosis.

In the rest of the world, other Amblyomma ticks serve as vectors for multiple species of Ehrlichia, including new genetic variants classified as Candidatus Neoehrlichia species in Europe and Asia. For veterinarians, heartwater disease, caused by Ehrlichia ruminantium, is an increasingly important reportable disease of ruminants in Africa and the Caribbean.

Viral Vector-Borne Diseases

Vector-borne viruses are another emerging global zoonotic threat. Many tick species carry viruses of increasing public health importance:

  • Rhipicephalus microplus and Haemaphysalis longicornis ticks in China and Amblyomma americanum in the United States are known vectors of closely related viruses causing severe fever and thrombocytopenia. In the United States, this virus is known as heartland virus.
  • Bourbon virus was recently discovered in the United States.
  • Powassan virus is reemerging in North America.
  • Tickborne encephalitis viruses are broadening in range throughout Europe as reforestation and movement of dogs allows the range of their vector, Dermacentor reticulatus, to expand into Germany, the Netherlands, and Poland.
  • Crimean-Congo hemorrhagic fever virus is spreading to multiple countries in the Mediterranean, likely due to the transportation of its tick vector, Hyalomma marginatum, by birds from Africa, Asia, and Eastern Europe to Central Europe.
Take-Home Message

Practitioners in both veterinary and human medicine must remain aware of the changing geography of ticks and associated vector-borne diseases. The discovery of the Asian tick H longicornis in New Jersey and Virginia should be an important reminder of the fact that

“ticks and tickborne pathogens do not recognize international boundaries.”

Thus, “a robust international disease monitoring network” is needed to protect both human and animal health from both known and emerging tick-borne diseases.
Dr. Boatright, a 2013 graduate of the University of Pennsylvania, is an associate veterinarian in western Pennsylvania. She is actively involved in her state and local veterinary medical associations and is a former national officer of the Veterinary Business Management Association.



Independent Canadian tick researcher states it’s migrating birds and photoperiod allowing tick populations to spread, not climate issues:

This groundbreaking study: shows a 85% probability for multiple infections in patients suffering from tick borne disease, including not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses.

Key Quote:

“Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.”

Eighty three percent of all commercial tests focus only on Lyme (borrelia), despite the fact we are infected with more than one microbe. It takes 11 different visits to 11 different doctors, utilizing 11 different tests to be properly diagnosed.

Time for things to change.



Prophage-driven Genomic Structural Changes Promote Bartonella Vertical Evolution

Prophage-driven genomic structural changes promote Bartonella vertical evolution

Genome Biology and Evolution, evy236,
22 October 2018


Bartonella is a genetically diverse group of vector-borne bacteria. Over 40 species have been characterized to date, mainly from mammalian reservoirs and arthropod vectors. Rodent reservoirs harbor one of the largest Bartonella diversity described to date, and novel species and genetic variants are continuously identified from these hosts. Yet, it is still unknown if this significant genetic diversity stems from adaptation to different niches or from intrinsic high mutation rates. Here, we explored the vertical occurrence of spontaneous genomic alterations in 18 lines derived from two rodent-associated Bartonella elizabethae-like strains, evolved in non-selective agar plates under conditions mimicking their vector- and mammalian-associated temperatures, and the transmission cycles between them (i.e. 26 °C, 37 °C, and alterations between the two), using mutation accumulation experiments.

After ∼1000 generations, evolved genomes revealed few point mutations (average of one-point mutation per line), evidencing conserved single-nucleotide mutation rates. Interestingly, three large structural genomic changes (two large deletions and an inversion) were identified over all lines, associated with prophages and surface adhesin genes. Particularly, a prophage, deleted during constant propagation at 37 °C, was associated with an increased autonomous replication at 26 °C (the flea-associated temperature). Complementary molecular analyses of wild strains, isolated from desert rodents and their fleas, further supported the occurrence of structural genomic variations and prophage-associated deletions in nature. Our findings suggest that structural genomic changes represent an effective intrinsic mechanism to generate diversity in slow-growing bacteria and emphasize the role of prophages as promoters of diversity in nature.



Bacteriophages or simply phages were discovered in the early 1900’s and are viruses which infect a bacterium causing horizontal gene transfer which in turn causes bacterial evolution.  

If you don’t know it yet, what goes into a Lyme/MSIDS patient is not what comes out.  These critters morph inside us turning into something quite different, which is one reason this complex is so difficult to treat.

When I read a book on antibiotic resistance, thankfully something that is not occurring yet in Lyme/MSIDS with few exceptions, I learned of phage therapy.  If this interests you check this out (located in the Republic of Georgia):

News articles on phage therapy:

I’ve been told phage therapy wouldn’t work with Lyme/MSIDS due to the lack of host specificity.  In other words, the phage must directly line up with the specific bacteria in order to work.  Also, most of us are dealing with more than one bacteria, and battle worms, parasites, and other lovely beasts thrown into the mix to keep us humble.

The take home from this abstract is that the bacteria we are infected with are intelligent and stealthy, changing within us to further their goals.  They don’t want to kill us, just maim and weaken us so they can live long, full lives.  Also, notice “slow-growing bacteria,” which should serve as a clue to practitioners that these types of organisms scoff at 21 days of antibiotics.

Diagnosing & Treating Autoimmune Encephalitis in Patients with Persistent Lyme Symptoms

 Approx. 47 Min.

Dr. Frid: Diagnosing and Treating Infectious Induced AE in Patients with Persistent Lyme Symptoms

Dr. Elena Frid talk Diagnosing and Treating Infections Induced Autoimmune Encephalitis in Patient’s with Persistent Lyme Symptoms to physicians and patients at the Central Mass Lyme conference


More with Dr. Frid:

More on Lyme encephalitis:  There is often involvement with Lyme/MSIDS in both Autism and PANS.  Here we see a story of Patrik, who was diagnosed with Lyme Disease which then morphs into Autoimmune encephalopathy. It took 10 years and 20 doctors to obtain the Lyme disease diagnosis behind his autoimmune condition.

How many people are slipping through this crack?

This pivotal study shows the complex issue of coinfections and the Lyme persister organism in lowering patients’ immune system thereby opening the door to opportunistic infections which can cause encephalopathy:




Hawk Found Carrying Asian Long-horned Tick – the One that Drains Cattle of all Their Blood  (News story found here)

It’s confirmed.  The tick from hell has been found on a hawk in Virginia.  

This Asian “dracula” tick causes SFTS (severe fever with thrombocytopenia syndrome), “an emerging hemorrhagic fever,” causing  fever, fatigue, headache, nausea, muscle pain, diarrhea, vomiting, abdominal pain, disease of the lymph nodes, and conjunctival congestion, but the potential impact of this tick on tickborne illness is not yet known. In other parts of the world, this Longhorned tick, also called the East Asian or bush tick, and has been associated with several tickborne diseases, such as spotted fever rickettsioses, Anaplasma, Ehrlichia, and Borrelia, the causative agent of Lyme Disease.

Main concerns:

  2. It can drain cattle of their blood:
  3. It’s been known to cause disease in Asia
  4. A top ecologist wonders if infection by this tick has gone undetected in the past.
  5. There isn’t a systematic national method to look for invasive ticks.
  6. It’s quickly showing up in other states:
  7. It survives cold temps: (Again, the spread if ticks and infection has ZIPPO to do with climate change)  Tick guy, Tom Mather, found that this particular tick, which reproduces by cloning itself, lines up on a single blade of grass motionless, tightly knitted together like the scales on a snake.  Once they found one glad of grass like this, they started seeing this every couple of feet.  He quickly realized this is NOT a rare tick.



Study Shows Lyme/MSIDS Patients Infected With Many Pathogens and Explains Why We Are So Sick (Please see comment at end of article)

Evaluating polymicrobial immune responses in patients suffering from tick-borne diseases

Kunal Garg, Leena Meriläinen, Ole Franz, Heidi Pirttinen, Marco Quevedo-Diaz, Stephen Croucher & Leona Gilbert
Scientific Reportsvolume 8, Article number: 15932 (2018)

There is insufficient evidence to support screening of various tick-borne diseases (TBD) related microbes alongside Borrelia in patients suffering from TBD. To evaluate the involvement of multiple microbial immune responses in patients experiencing TBD we utilized enzyme-linked immunosorbent assay. Four hundred and thirty-two human serum samples organized into seven categories followed Centers for Disease Control and Prevention two-tier Lyme disease (LD) diagnosis guidelines and Infectious Disease Society of America guidelines for post-treatment Lyme disease syndrome. All patient categories were tested for their immunoglobulin M (IgM) and G (IgG) responses against 20 microbes associated with TBD. Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes. We have established a causal association between TBD patients and TBD associated co-infections and essential opportunistic microbes following Bradford Hill’s criteria. This study indicated an 85% probability that a randomly selected TBD patient will respond to Borrelia and other related TBD microbes rather than to Borrelia alone.

A paradigm shift is required in current healthcare policies to diagnose TBD so that patients can get tested and treated even for opportunistic infections.
Please see link for full article.  Snippets below:

Tick-borne diseases (TBDs) have become a global public health challenge and will affect over 35% of the global population by 20501. The most common tick-borne bacteria are from the Borrelia burgdorferi sensu lato (s.l.) group. However, ticks can also transmit co-infections like Babesia spp.2, Bartonella spp.3, Brucella spp.4,5,6,7,8, Ehrlichia spp.9, Rickettsia spp.10,11, and tick-borne encephalitis virus12,13,14. In Europe and North America, 4–60% of patients with Lyme disease (LD) were co-infected with Babesia, Anaplasma, or Rickettsia11,15,16. Evidence from mouse and human studies indicate that pathogenesis by various tick-borne associated microbes15,16,17 may cause immune dysfunction and alter, enhance the severity, or suppress the course of infection due to the increased microbial burden18,19,20,21,22. As a consequence of extensive exposure to tick-borne infections15,16,17, patients may develop a weakened immune system22,23, and present evidence of opportunistic infections such as Chlamydia spp.24,25,26,27, Coxsackievirus28, Cytomegalovirus29, Epstein-Barr virus27,29, Human parvovirus B1924, and Mycoplasma spp.30,31. In addition to tick-borne co-infections and non-tick-borne opportunistic infections, pleomorphic Borrelia persistent forms may induce distinct immune responses in patients by having different antigenic properties compared to typical spirochetes32,33,34,35. Nonetheless, current LD diagnostic tools do not include Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic infections.

The two-tier guidelines36,37,38 for diagnosing LD by the Centers for Disease Control and Prevention (CDC) have been challenged due to the omission of co-infections and non-tick-borne opportunistic infections crucial for comprehensive diagnosis and treatment39,40. Emerging diagnostic solutions have demonstrated the usefulness of multiplex assays to test for LD and tick-borne co-infections41,42. However, these new technologies do not address seroprevalence of non-tick-borne opportunistic infections in patients suffering from TBD and they are limited to certain co-infections41,42. Non-tick-borne opportunistic microbes can manifest an array of symptoms24,29 concerning the heart, kidney, musculoskeletal, and the central nervous system as seen in patients with Lyme related carditis43, nephritis44, arthritis45, and neuropathy46, respectively. Therefore, Chlamydia spp., Coxsackievirus, Cytomegalovirus, Epstein-Barr virus, Human parvovirus B19, Mycoplasma spp., and other non-tick-borne opportunistic microbes play an important role in the differential diagnosis of LD24,29. As the current knowledge regarding non-tick-borne opportunistic microbes is limited to their use in differential diagnosis of LD, it is unclear if LD patients can present both tick-borne co-infections and non-tick-borne opportunistic infections simultaneously.

For the first time, we evaluate the involvement of Borrelia spirochetes, Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic microbes together in patients suffering from different stages of TBD. To highlight the need for multiplex TBD assays in clinical laboratories, we utilized the Bradford Hill’s causal inference criteria47 to elucidate the likelihood and plausibility of TBD patients responding to multiple microbes rather than one microbe. The goal of this study is to advocate screening for various TBD microbes including non-tick-borne opportunistic microbes to decrease the rate of misdiagnosed or undiagnosed48 cases thereby increasing the health-related quality of life for the patients39, and ultimately influencing new treatment protocol for TBDs.

Positive IgM and IgG responses by CDC defined acute, CDC late, CDC negative, PTLDS immunocompromised, and unspecific patients to 20 microbes associated with TBD (Fig. 1) were utilized to evaluate polymicrobial infections (Figs 2–4). Patient categories included CDC acute (n = 43), CDC late (n = 43), CDC negative (n = 46), PTLDS (n = 31), immunocompromised (n = 61), unspecific (n = 31), and healthy (n = 177).

Polymicrobial infections are present at all stages of tick-borne diseases.

Microbes include Borrelia burgdorferi sensu stricto, Borrelia afzelii, Borrelia garinii, Borrelia burgdorferi sensu stricto persistent form, Borrelia afzelii persistent form, Borrelia garinii persistent form, Babesia microti, Bartonella henselae, Brucella abortus, Ehrlichia chaffeensis, Rickettsia akari, Tick-borne encephalitis virus (TBEV), Chlamydia pneumoniae, Chlamydia trachomatis, Coxsackievirus A16 (CVA16), Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Mycoplasma pneumoniae, Mycoplasma fermentans, and Human parvovirus B19 (HB19V).

In Fig. 2A, 51% and 65% of patients had IgM and IgG responses to more than one microbe, whereas 9% and 16% of patients had IgM and IgG responses to only one microbe, respectively. Immune responses to Borrelia persistent forms (all three species) for IgM and IgG were 5–10% higher compared to Borrelia spirochetes in all three species (Fig. 2B). Interestingly, the probability that a randomly selected patient will respond to Borrelia persistent forms rather than the Borrelia spirochetes (Fig. S2) is 80% (d = 1.2) for IgM and 68% for IgG (d = 0.7). Figure 2A and B indicated that IgM and IgG responses by patients from different stages of TBDs are not limited to only Borrelia spirochetes.

In Fig. 3 sub-inlets, more than 50% of the patients reacted to only the individual Borrelia strains suggesting that Borrelia antigens are not cross-reactive. If patients were cross-reacting among antigens, a larger percentage of the patients would be seen with the combination of all three species (Fig. S2). These results provide evidence to suggest that the inclusion of different Borrelia species and their morphologies in current LD diagnostic tools will improve its efficiency.

The study outcome indicated that polymicrobial infections existed at all stages of TBD with IgM and IgG responses to several microbes (Fig. 2). Results presented in this study propose that infections in patients suffering from TBDs do not obey the one microbe one disease Germ Theory. Based on these results and substantial literature11,15,16,17,27,49,50,51 on polymicrobial infections in TBD patients, we examined the probability of a causal relationship between TBD patients and polymicrobial infections following Hill’s nine criteria47.

An average effect size of d = 1.5 for IgM and IgG (Fig. 4A) responses is considered very large52. According to common language effect size statistics53, d = 1.5 indicates 85% probability that a randomly selected patient will respond to Borrelia and other TBD microbes rather than to only Borrelia. Reports from countries such as Australia27, Germany49, Netherlands11, Sweden50, the United Kingdom51, the USA15,16, and others indicate that 4% to 60% of patients suffer from LD and other microbes such as Babesia microti and human granulocytic anaplasmosis (HGA). However, previous findings11,15,16,27,49,50,51 are limited to co-infections (i.e., Babesia, Bartonella, Ehrlichia, or Rickettsia species) in patients experiencing a particular stage of LD (such as Erythema migrans). In contrast, a broader spectrum of persistent, co-infections, and opportunistic infections associated with diverse stages of TBD patients have been demonstrated in this study (Fig. 2). From a clinical standpoint, the likelihood for IgM and IgG immune responses by TBD patients to the Borrelia spirochetes versus the Borrelia persistent forms, and responses to just Borrelia versus Borrelia with many other TBD microbes has been quantified for the first time (Fig. S2).

Borrelia pathogenesis could predispose individuals to polymicrobial infections because it can suppress, subvert, or modulate the host’s immune system18,19,20,21,22 to create a niche for colonization by other microbes54. Evidence in animals55 and humans11,15,16,27,49,50,51 frequently indicate co-existence of Borrelia with other TBD associated infections. Interestingly, IgM and IgG immune levels by patients to multiple forms of Borrelia resulted in immune responses to 14 other TBD microbes (Fig. 4B). In contrast, patient responses to either form of Borrelia (spirochetes or persistent forms) resulted in reactions to an average of 8 other TBD microbes (Fig. 4B). Reaction to two forms of Borrelia reflected an increase in disease severity indicating biological gradient for causation as required by Hill’s criteria47.

Multiple microbial infections in TBD patients seem plausible because ticks can carry more than eight different microbes depending on tick species and geography56,57. Moreover, Qiu and colleagues reported the presence of at least 18 bacterial genera shared among three different tick species and up to 127 bacterial genera in Ixodes persulcatus58. Interestingly, research indicates Chlamydia-like organism in Ixodes ricinus ticks and human skin59 that may explain immune responses to Chlamydia spp., seen in this study (Fig. 2). Additionally, prevalence of TBD associated co-infections such as B. abortus, E. chaffeensis, and opportunistic microbes such as C. pneumoniae, C. trachomatis, Cytomegalovirus, Epstein-Barr virus, and M. pneumoniae have been recorded in the general population of Europe and the USA (Table S2). However, true incidence of these microbes is likely to be higher considering underreporting due to asymptomatic infections and differences in diagnostic practices and surveillance systems across Europe and in the USA. More importantly, clinical evidence for multiple microbes has been reported in humans11,15,16,27,49,50,51, and livestock55 to mention the least. Our findings regarding the presence of polymicrobial infections at all stages of TBD further supports the causal relationship between TBD patients and polymicrobial infections (Fig. 2). Various microbial infections in TBD patients have been linked to the reduced health-related quality of life (HRQoL) and increased disease severity39.

An association between multiple infections and TBD patients relates well to other diseases such as periodontal, and respiratory tract diseases. Oral cavities may contain viruses and 500 different bacterial species60. Our findings demonstrate that TBD patients may suffer from multiple bacterial and viral infections (Fig. 4). In respiratory tract diseases, influenza virus can stimulate immunosuppression and predispose patients to bacterial infections causing an increase in disease severity61. Likewise, Borrelia can induce immunosuppression that may predispose patients to other microbial infections causing an increase in disease severity.

Traditionally, positive IgM immune reaction implies an acute infection, and IgG response portrays a dissemination, persistent or memory immunity due to past infections. Depending on when TBD patients seek medical advice, the level of anti-Borrelia antibodies can greatly vary as an Erythema migrans (EM) develops and may present with IgM, IgG, collective IgM/IgG, or IgA62. This study recommends both IgM and IgG in diagnosing TBD (Figs 5 and S4–S6) as unconventional antibody profiles have been portrayed in TBD patients. Presence of long-term IgM and IgG antibodies have been reported in LD patients that were tested by the CDC two-tier system. In 2001, Kalish and colleagues reported anti-Borrelia IgM or IgG persistence in patients that suffered from LD 10–20 years ago63. Similarly, Hilton and co-workers recorded persistent anti-Borrelia IgM response in 97% of late LD patients that were considered cured following an antibiotic treatment64.

Similar events of persistent IgM and IgG antibody reactions were demonstrated in patients treated for Borrelia arthritis and acrodermatitis chronica atrophicans65, chronic cutaneous borreliosis66, and Lyme neuroborreliosis67. A clear phenomenon of immune dysfunction is occurring, which might account for the disparities in LD patient’s antibody profiles and persistence. Borrelia suppresses the immune system by inhibition of antigen-induced lymphocyte proliferation18, reducing Langerhans cells by downregulation of major histocompatibility complex class II molecules on these cells19, stimulating the production of interleukin-10 and anti-inflammatory immunosuppressive cytokine20, and causing disparity in regulation and secretion of cytokines21. Other studies have demonstrated low production or subversion of specific anti-Borrelia antibodies in patients with immune deficiency status22.

In the USA alone, the economic healthcare burden for patients suffering from LD and ongoing symptoms is estimated to be $1.3 billion per year69. Additionally, 83% of all TBD diagnostic tests performed by the commercial laboratories in the USA accounted for only LD70. Globally, the commercial laboratories’ ability to diagnose LD has increased by merely 4% (weighted mean for ELISA sensitivity 62.3%) in the last 20 years71. This study provides evidence regarding polymicrobial infections in patients suffering from different stages of TBDs. Literature analyses and results from this study followed Hill’s criteria indicating a causal association between TBD patients and polymicrobial infections. Also, the study outcomes indicate that patients may not adhere to traditional IgM and IgG responses.



For the first time, Garg et al. show a 85% probability for multiple infections including not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses.

I’m thankful they included Bartonella as that one is often omitted but definitely a player.  I’m also thankful for the mention of viruses as they too are in the mix.  The mention of the persister form must be recognized as well as many out there deny its existence.

Key Quote:  Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.”

But there is another important point.

According to this review, 83% of all commercial tests focus only on Lyme (borrelia), despite the fact we are infected with more than one microbe.  The review also states it takes 11 different visits to 11 different doctors, utilizing 11 different tests to be properly diagnosed.

This is huge.  Please spread the word.


Why Everything You Learned About Viruses is Wrong

Why Everything You Learned About Viruses Is WRONG

Groundbreaking research indicates that most of what we believed about the purportedly deadly properties of viruses like influenza is based on nothing more than institutionalized superstition and myth. 

Germ theory is an immensely powerful force on this planet, affecting everyday interactions from a handshake, all the way up the ladder to national vaccination agendas and global eradication campaigns.

But what if fundamental research on what exactly these ‘pathogens’ are, how they infect us, has not yet even been performed? What if much of what is assumed and believed about the danger of microbes, particularly viruses, has completely been undermined in light of radical new discoveries in microbiology?

Some of our readers already know that in my previous writings I discuss why the “germs as our enemies” concept has been decimated by the relatively recent discovery of the microbiome. For in depth background on this topic, read my previous article, “How The Microbiome Destroyed the Ego, Vaccine Policy, and Patriarchy.” You can also read Profound Implications of the Virome for Human Health and Autoimmunity, to get a better understanding of how viruses are actually benefificial to health.

In this article I will take a less philosophical approach, and focus on influenza as a more concrete example of the Copernican-level paradigm shift in biomedicine and life sciences we are all presently fully immersed within, even if the medical establishment hs yast to acknowledge it.

Deadly Flu Viruses: Vaccinate or Die?

The hyperbolic manner in which health policymakers and the mainstream media talk about it today, flu virus is a deadly force, against which all citizens, of all ages 6 months or older, need to take an annual influenza vaccine to protect themselves against, lest they face deadly consequences. Worse, those who hold religious or philosophical objections, or who otherwise conscientiously object to vaccinating, are being characterized as doing harm to others by denying them herd immunity (a concept that has been completely debunked by a careful study of the evidence, or lack thereof). For instance, in the interview below Bill Gates tells Sanjay Gupta that he thinks non-vaccinators “kill children”:

But what if I told you that there isn’t even such a thing as “flu virus,” in the sense of a monolithic, disease vector existing outside of us, conceived as it is as the relationship of predator to prey?

First, consider that the highly authorative Cochrane collaboration acknowledges there are many different flu viruses that are not, in fact, influenza A — against which flu vaccines are targeted — but which nonetheless can contribute to symptoms identical to those attributed to influenza A:

Over 200 viruses cause influenza and influenza-like illness which produce the same symptoms (fever, headache, aches and pains, cough and runny noses). Without laboratory tests, doctors cannot tell the two illnesses apart. Both last for days and rarely lead to death or serious illness. At best, vaccines might be effective against only Influenza A and B, which represent about 10% of all circulating viruses.” (Source: Cochrane Summaries).” [emphasis added]

This makes for a picture of complexity that powerfully undermines health policies that presuppose vaccination equates to bona fide immunity, and by implication, necessitates the herd collectively participate in the ritual of mass vaccination campaigns as a matter of social responsibility and necessity.

Even the use of the word “immunization” to describe vaccination is highly misleading. The moment the word is used, it already presupposes efficacy, and makes it appear as if non-vaccinators are anti-immunity, instead of what they actually are: pro-immunity (via clean air, food, water, and sunlight), but unwilling to subject themselves or their healthy children to “unavoidably unsafe” medical procedures with only theoretical benefits.

Why Flu Virus Doesn’t Exist (The Way We Were Told)

But the topic gets even more interesting when we consider the findings of a 2015 study entitled “Conserved and host-specific features of influenza vision architecture.” This was the first study ever to plumb the molecular depths of what influenza virus is actually composed of. Amazingly, given the long history of vaccine use and promotion, the full characterization of what proteins it contains, and where they are derived from, was never previously performed. How we invest billions of dollars annually into flu vaccines, and have created a global campaign to countermand a viral enemy, whose basic building blocks we don’t even know, is hard to understand. But it is true nonetheless.

The study abstract opens with this highly provocative line:

“Viruses use virions to spread between hosts, and virion composition is therefore the primary determinant of viral transmissibility and immunogenicity.” [emphasis added]

Virion are also known as “viral particles,” and they are the means by which viral nucleic acids are able to move and ‘infect’ living organisms. Without the viral particle (taxi) to carry around the virus DNA (passenger), it would be harmless; in fact, viruses are often described as existing somewhere between living and inanimate objects for this reason: they do not produce their own energy, nor are transmissable without a living host. And so, in this first line, the authors are making it clear that virion composition is also the primary determinant in how or whether a virus is infectious (transmits) and what affects it will have in the immune system of the infected host.

Influenza viral particles.

This distinction is important because we often think of viruses as simply pathogenic strings of DNA or RNA. The irony, of course, is that the very things we attribute so much lethality to — viral nucleic acids — are not even alive, and can not infect an organism without all the other components (proteins, lipids, extra-viral nucleic acids) which are, technically, not viral in origin, participating in the process. And so, if the components that are non-viral are essential for the virus to cause harm, how can we continue to maintain that we up against a monolithic disease entity “out there” who “infects” us, a passive victim?  It’s fundamentally non-sensical, given these findings. It also clearly undermines the incessant, fear-based rhetoric those beholden to the pro-vaccine use to coerce the masses into undergoing the largely faith-based rite of vaccination. 

Let’s dive deeper into the study’s findings…

The next line of the abstract addresses the fact we opened this article with: namely, that there is great complexity involved at the level of the profound variability in virion composition:

“However, the virions of many viruses are complex and pleomorphic, making them difficult to analyze in detail”

But this problem of the great variability in the virion composition of influenza is exactly why the study was conducted. They explain:

“Here we address this by identifying and quantifying viral proteins with mass spectrometry, producing a complete and quantifiable model of the hundreds of viral and host-encoded proteins that make up the pleomorphic virions of influenza virus.  We show that a conserved influenza virion architecture, which includes substantial quantities of host proteins as well as the viral protein NSI, is elaborated with abundant host-dependent features. As a result, influenza virions produced by mammalian and avian hosts have distinct protein compositions.”

In other words, they found that the flu virus is as much comprised of biological material from the host the virus ‘infects,’ as the viral genetic material of the virus per se.

How then, do we differentiate influenza virus as fully “other”? Given that it would not exist without “self” proteins, or those of other host animals like birds (avian) or insects, this would be impossible to do with any intellectual honesty intact.

There’s also the significant problem presented by flu vaccine production. Presently, human flu vaccine antigen is produced via insects and chicken eggs. This means that the virus particles extracted from these hosts would contain foreign proteins, and would therefore produce different and/or unpredictable immunological responses in humans than would be expected from human influenza viral particles. One possibility is that the dozens of foreign proteins found within avian influenza could theoretically produce antigens in humans that cross-react with self-structures resulting in autoimmunity. Safety testing, presently, does not test for these cross reactions. Clearly, this discovery opens up a pandora’s box of potential problems that have never sufficiently been analyzed, since it was never understood until now that “influenza” is so thoroughly dependent upon a host for its transmissability and immunogenecity.

Are Flu Viruses Really “Hijacked” Exosomes?

Lastly, the study identified something even more amazing:

“Finally, we note that influenza virions share an underlying protein composition with exosomes, suggesting that influenza virions form by subverting micro vesicle” production.”

What these researchers are talking about is the discovery that virion particles share stunning similarities to naturally occurring virus-like particles produced by all living cells called exosomes. Exosomes, like many viruses (i.e. enveloped viruses) are enclosed in a membrane, and are within the 50-100 nanometer size range that viruses are (20-400 nm). They also contain biologically active molecules, such as proteins and lipids, as well as information-containing ones like RNAs — exactly, or very similar, to the types of contents you find in viral particles.

Watch this basic video on exosomes to get a primer:

When we start to look at viruses through the lens of their overlap with exosomes, which as carriers of RNAs are essential for regulating the expression of the vast majority of the human genome, we start to understand how their function could be considered neutral as “information carriers,” if not beneficial. Both exosomes and viruses may actually be responsible for inter-species or cross-kingdom communication and regulation within the biosphere, given the way they are able to facilitate and mediate horizontal information transfer between organisms. Even eating a piece of fruit containing these exosomes can alter the expression of vitally important genes within our body.


In light of this post-Germ Theory perspective, viruses could be described as pieces of information in search of chromosomes; not inherently “bad,” but, in fact, essential for mediating the genotype/phenotype relationship within organisms, who must adapt to ever-shifting environmental conditions in real-time in order to survive; something the glacial pace of genetic changes within the primary nucleotide sequences of our DNA cannot do (for instance, it may take ~ 100,000 years for a protein-coding gene sequence to change versus seconds for a protein-coding gene’s expression to be altered via modulation via viral or exosomal RNAs).

This does not mean they are “all good,” either. Sometimes, given many conditions outside their control, their messages could present challenges or misinformation to the cells to which they are exposed, which could result in a “disease symptom.” But with the caveat that these disease symptoms are often if not invariably attempts by the body to self-regulate and ultimately improve and heal itself.

In other words, the virion composition of viruses appears to be the byproduct of the cell’s normal exosome (also known as microvessicle) production machinery and trafficking, albeit being influenced by influenza DNA. And like exosomes, viruses may be a means of extracellular communication between cells, instead of simply a pathological disease entity.  This could explain why an accumulating body of research on the role of the virome in human health indicates that so-called infectious agents, including viruses like measles, confer significant health benefits. [see: the Health Benefits of Measles and TheHealing Power of Germs?].

Other researchers have come to similar discoveries about the relationship between exosomes and viruses, sometimes describing viral hijacking of exosome pathways as a “Trojan horse” hypothesis.  HIV may provide such an example.

Concluding Remarks

The remarkably recent discovery of the host-dependent nature of the influenza virus’ virion composition is really just the tip of an intellectual iceberg that has yet to fully emerge into the light of day, but is already “sinking” ships; paradigm ships, if you will.

One such paradigm is that germs are enemy combatants, and that viruses serve no fundamental role in our health, and should be eradicated from the earth with drugs and vaccines, if possible.

This belief, however, is untenable. With the discovery of the indispensable role of the microbiome, and the subpopulation of viruses within it — the virome — we have entered into an entirely new, ecologically-based view of the body and its environs that are fundamentally inseparable. Ironically, the only thing that influenza may be capable of killing is germ theory itself. 

For an in-depth exploration of this, watch the lecture below on the virome. I promise, if you do so, you will no longer be able to uphold germ theory as a monolithic truth any longer. You may even start to understand how we might consider some viruses “our friends,” and why we may need viruses far more than they need us.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.  (EBV – A Key Player in Chronic Illness & Tips to Treat Reactivated EBV)

Autism Spectrum Disorder (ASD) The Question Every Parent Should Ask….Why is This Not Medical?

Autism Spectrum Disorder (ASD) The Question Every Parent should ask.… Why is This Not Medical?

Michael Goldberg, MD

There are different kinds of childhood disorders, yet none scientifically or medically can remotely affect the CDC reported 1:36 children and be thought of as genetic or developmental in origin, unless, medical science is ignored and that child is NOW labeled, ASD Autistic! However, given the horrific and increasing numbers of ASD affected children, there must be an underlying unidentified medical disease presenting with autistic like symptoms and behaviors i.e. an ASD “PHENOTYPE”!  

It is scientifically impossible to have an epidemic without a disease origin. Mistakenly labeling and then treating children as “psychiatric Autistic” is the failure of our medical system to recognize these children are really part of an enlarging, unrecognized medical pandemic affecting children and young adults. ASD (1:36) today is worse than the Polio epidemic (1:1500 – 1:2000) of the 1950’s.

As early as the 1960s, certainly in the 1970s, pediatricians were being taught at UCLA and other excellent medical schools that Psychiatric, DSM autism affected 1 – 2 in 10,000 children. Further, those 1-2 children, in order to be labeled Autistic must never be affectionate/ never normal! To have that number mysteriously begin to increase in the 1990s to the astounding level of 1 in 36 otherwise affectionate children begs the questions; “Is this epidemic? And if so “Why is this condition not considered and treated as medical?”  

Instead of being excited about the arrival of new baby, watching a child grow and prosper, sadly many mother’s today (expressed constantly when meeting new parents) live with perhaps worse fears than parents and families of the 40s and 50s. At that time the polio epidemic was a real threat, affecting 1:1500 – 1:2000 children, and the world mobilized to find a cure. Today ASD affects 1:36 and climbing! Where is the medical community? You cannot have an epidemic of psychiatric or developmental conditions!

I am proposing an answer to the question, nobody in public health, academic research or the pediatric medical community dare to acknowledge or ask: Is ASD in children and young adults a medical condition? Are they medically ill and thus treatable? 

 My answer: YES and the medically treatable symptoms and manifestations are directly related to Herpes viruses (potentially others) and the immune system! 

Medical School of the 1970s was eventful.  Professors opined we were entering a “golden age” of medicine, because “common” pathogens were being identified and eradicated. As new physicians we recognized we live in a sea of viruses. We were protected by our immune system and its adaption over thousands of years.

Nobel level professors taught there were differences between “normal” viral titers (markers) and “elevated” viral titers, indicating the presence of an active virus. Then in the early – mid 1980s very powerful medical leaders (CDC, NIH) unexplainably decided elevated Herpes viral titers in children and adults were meaningless! Lab evaluations of “normal” vs. elevated, are still carried over today, but “ignored” when elevated. As a practicing pediatrician, to suddenly be required to ignore the role of the Herpes virus was and still is beyond comprehension.  

The Medical Literature still support the significance of a fourfold change in viral titers. However, if a pediatrician does not consider or is precluded from testing for viral titers, how can the physician begin to evaluate or “rule out” if there is treatable viral activity? She/he cannot! How does that benefit the child or the family? It does not! For a physician to leave a child with overwhelming sensory issues, without a complete medical work up is unconscionable. In my opinion, to discount and ignore elevated viral titers in children and young adults remains one of the biggest travesties being perpetrated upon our children by the current medical system.

All of the ASD labeled children I am working up are affectionate. Many present with this ASD “phenotype”. Typically, their blood tests show elevated viral titers for the HHV6 herpes virus, Epstein Barr and/or CMV virus. In addition, many of these children also present with outright early developmental delays and motor issues. For these issues, I was taught by excellent professors to think of viruses, “rule-out viruses.”  

Most children having issues today become labeled as “on the ASD spectrum” without a proper medical workup and investigation for illness, chronic viral activation issues, etc. By artificially removing the medical criteria developed over decades past, the current “system” too quickly, attaches the label of ASD. The pediatrician unwittingly abandons the children and parents to the psychiatric community for behavior training and a life of isolation and despair. Parents are told to cope and forego their focus or desire to pursue real medical answers and real potential help for their children. How much worse can this get before parents and others step up and declare “enough is enough”!

In my professional opinion based upon over 40+ years of clinical experience, “Autism spectrum disorder” (not meeting strict Kanner criteria) with accompanying language impairment is in reality a medical disease (complex immune – complex viral) presenting as an encephalopathy (often viral) with “autistic” symptoms.

The language impairment in these ASD labeled children is part of the disease, not secondary to Autism Spectrum Disorder. Many of my patients (approx. 75+%) respond favorably to a medical protocol of anti-viral medications and diet modifications, eliminating known allergenic foods. This anti-viral component mitigates the effects of the viruses to the brain, while the diet changes reduce stress on the body, the brain, and the immune system. Additional improvement is achieved with the use of an SSRI (Selective Serotonin Reuptake Inhibitor). The SSRI is introduced not for “depression,” but as a pharmaceutical/medical way to treat temporal lobe hypo perfusion; a real, medically definable, physiologic CNS dysfunction evidenced on a NeuroSPECT scan

This medical protocol results in the elimination or severe abatement of the “autistic” like symptoms and behaviors and allows an increase in, a return of, higher cognitive function. The most common phrase I hear from parents of improving children is,

“It is as if a fog has lifted.”

and from speech and other therapists,

“This is not the same child I have been working with.”

These otherwise affectionate “typical/normal” (now much brighter cognitively) children are now placed in a position to be taught (not trained), allowed to “catch up” and progress with their peers. For whatever reasons, those in positions of authority refuse to acknowledge or investigate this treatable complex immune, complex viral medical problem. Instead, current focus and research is on “causation” with activated “gene expressions” or “complex genetic” ideas being proffered as the origin. The reality is a treatable underlying viral/immune process is being ignored! The “system” has become so biased, against the obvious, that good professors wishing to pursue research into a readily treatable complex immune, complex viral causation, have not only been refused funding, but fear losing their positions. These short-sighted money decisions at the clinical level mean the loss of the near immediate relief from ASD behaviors and mannerisms, improved, often excellent cognitive abilities, and improvement in the future quality of life for the child and family. Why?

Recently I met with a group of educators discussing the “differences” working with a medically treated ASD child (stressing an ASD “phenotype,” not developmental “autism”). They were aware the medically treated child was able to understand and be taught! These educators realized this was an emerging potentially regular child, not a child mysteriously born “miss-wired.” Thankfully, there are excellent academic professors who also know something is seriously wrong, literally acknowledging we are in a missed medical “pandemic”.

An appropriately focused and engaged medical community together with key medical and academic researchers, could create a pathway for a healthier future for the children and reduce the financial costs to all affected, including our social and educational systems.



The Duke study is remarkable in that 60-70% or more of children with Autism have de novo gene mutations (not found in either parent) that must have occurred after birth according to the results, not in the egg, sperm or early utero development as previously, and erroneously assumed.  This new finding reveals research should now be geared to finding out what environmental damage after birth leads to these mutations and/or what pathogens are acting as triggers.  Autism like Lyme/MSIDS is a pandemic and according to one Wisconsin LLMD, 80% of his Autistic patients are also infected with Lyme/MSIDS.

More and more is coming out about the pathogenic aspect of disease (even mental illness).  This is certainly true for Alzheimer’s & Dementia, as well as other autoimmune issues such as in this story:  While Susannah Cahalan’s issue was truly autoimmune, we learn of Patrik, who had Lyme:

Boy’s Lyme Disease Morphs into Autoimmune encephalopathy. It took 10 years and 20 doctors to find out 12-year-old Patrik had Lyme disease. Just 4 months later the doctors discovered he also has a condition where his immune system attacks his brain. Dr. Souhel Najjar, Cahalan’s doctor, heroically saves the day again.

This is another great read regarding the pathogen element within Alzheimer’s:

Then there’s this gem:  (Excerpt below)

MacDonald states that both worms and borrelia can cause devastating brain damage and that,


“while patients are wrongly declared free of Lyme and other tick-borne infections, in reality, too often they contract serious neurodegenerative diseases which can kill them.”

MacDonald made his discovery from 10 specimens from the Rocky Mountain Multiple Sclerosis Center Tissue Bank. All 10 showed evidence of borrelia infected nematodes. Five patients who died of Glioblastoma multiforme, a malignant brain tumor, and four patients who died of Lewy Body dementia also showed infected nematodes.  MacDonald used FISH, Fluorescent In Situ Hybridization, which uses molecular beacon DNA probes to identify pieces of borrelia’s genetic material which fluoresce under the microscope with a 100% DNA match.

In other words, this is no mistake.