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RSV

Category: Illness or disabilities

Type

Involuntary

Introduction and description

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Human respiratory syncytial virus (RSV) is a virus that causes respiratory tract infections and lung diseases. It is a major cause of lower respiratory tract infections and hospital visits during infancy and childhood.

RSV is a negative-sense, single-stranded RNA virus of the family Paramyxoviridae, which includes common respiratory viruses such as those causing measles and mumps. RSV is a member of the paramyxovirus subfamily Pneumovirinae. Its name comes from the fact that F proteins on the surface of the virus cause the cell membranes on nearby cells to merge, forming syncytia.

It is a virus that exhibits latency.  In other words, even if the body develops an immune response, it can lie low in the body waiting for a time when the immune system is depressed and then re-emerge to produce disease.  The use of drugs such as immunosuppressants can thus trigger the reactivation of the virus.

There is mounting evidence that the RSV virus becomes latent or persists in vivo, but little is known about the mechanisms of its latency, persistence, and immune evasion. We therefore infected BALB/c mice intranasally with human RSV, analyzed sequential tissue samples by direct culture and polymerase chain reaction for viral and messenger RNA, and monitored antiviral immune responses. Virus could not be detected in bronchoalveolar lavage samples beyond Day 14, but viral genomic and messenger RNA was present in lung homogenates for 100 days or more; combined depletion of CD4 and CD8 T cells allowed infective virus to be recovered. Neutralizing antibody and memory cytotoxic T cell responses were intact in mice with latent infections, and latent viral genome contained an authentic nonmutated M2 82-91 K(d) cytotoxic T lymphocyte epitope. A mutation of this epitope, detected in one clone, did not assist evasion. We suggest that RSV latency depends on persistence in privileged sites rather than on viral mutation.  PMID:  14742302

Symptoms

 

The main symptom is ‘Bronchiolitis’ an inflammation of the bronchioles, the smallest air passages of the lungs. It presents with coughing, wheezing and shortness of breath.  Of those infected with RSV, 2–3% will develop bronchiolitis, necessitating hospitalization.

The virus appears to migrate principally to the lungs, but if the bloodbrain barrier has been compromised or the virus is able to enter the nose and then bypass the protection in the nose [for example due to the unwise use of nasal sprays], then the virus, in rare cases has been known to enter the brain.

We describe 4 nonconsecutive cases of infants admitted to Catholic University pediatric intensive care unit (PICU) because of complicated respiratory syncytial virus (RSV) infection during winter RSV outbreaks from the year 2000 to the year 2003. A hyponatremic epileptic status (as in the first case) has been reported by several authors as a rare RSV complication, potentially leading to death. PMID:  16912626

 

Hyponatremia (American English) or hyponatraemia (British English) is low sodium concentration in the blood.

As the virus is a latent virus, people can be infected multiple times. Sometimes an infant can become symptomatically infected more than once, even within a single RSV season.

Severe RSV infections have increasingly been found among elderly patients. Young adults can be re-infected every five to seven years, with symptoms looking like a sinus infection or a cold (infections can also be asymptomatic).

Long term effects

One of the major questions regarding long-term side effects of respiratory syncytial virus (RSV) is whether or not it induces asthma, lung diseases such as COPD or emphysema in later life. There are many causes of asthma, emphysema and lung diseases, as such it is extremely difficult to pinpoint whether the presence of RSV is a cause or an effect.

Asthma

 In this study a link was found with asthma:

Up to 5 y of follow-up after RSV bronchiolitis in infancy, 40% of children reported wheezing as compared to only 11% in the control group (p <0.001). Between 5 and 10 y of follow-up 22% of the bronchiolitis group reported wheezing against 10% of the control group (p = 0.19). The incidence of recurrent wheezing as defined by three or more wheezing episodes also decreased with increasing years of follow-up: at 5 or more years of follow-up the difference between the RSV group and the control group was no longer significant.  PMID:  10914957

The control group in this study has no real significance, as their asthma could have been caused by other pathogens.  What is clear is that RSV is linked to asthma in some way.

Emphysema and other lung diseases

 

Spontaneous pneumomediastinum is usually secondary to alveolar rupture in the pulmonary interstitium, associated with subcutaneous emphysema and occasionally with pneumothorax, but is rarely associated with pneumorrhachis. The leaked air into the pulmonary perivascular interstitium follows the path of least resistance from the mediastinum to the fascial planes of the neck. Air freely communicates via the neural foramina and collects in the epidural space. Pneumorrhachis is defined as the presence of air in the spinal canal, either in the intradural and/or extradural spaces. It is a very rare clinical entity and mostly asymptomatic, hence most probably underdiagnosed. Many pathological and physiological events can lead to alveolar rupture, and these clinical findings can be related to various, mainly traumatic and iatrogenic etiologies.

Herein we report three cases of pneumomediastinum, subcutaneous emphysema, interstitial emphysema and pneumorrhachis in two cases, which were related to rhinovirus, human bocavirus and respiratory syncytial virus infection. PMID: 26508192

COPD

Just like asthma and emphysema etc, COPD can also have more than one cause.  But again there is a definite link with RSV:

 

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation and/or airflow limitation due to pulmonary emphysema. Chronic bronchitis, pulmonary emphysema, and bronchial asthma may all be associated with airflow limitation; therefore, exacerbation of asthma may be associated with the pathophysiology of COPD. Furthermore, recent studies have suggested that the exacerbation of asthma, namely virus-induced asthma, may be associated with a wide variety of respiratory viruses. COPD and asthma have different underlying pathophysiological processes and thus require individual therapies. Exacerbation of both COPD and asthma, which are basically defined and diagnosed by clinical symptoms, is associated with a rapid decline in lung function and increased mortality. Similar pathogens, including human rhinovirus, respiratory syncytial virus, influenza virus, parainfluenza virus, and coronavirus, are also frequently detected during exacerbation of asthma and/or COPD. Immune response to respiratory viral infections, which may be related to the severity of exacerbation in each disease, varies in patients with both COPD and asthma. In this regard, it is crucial to recognize and understand both the similarities and differences of clinical features in patients with COPD and/or asthma associated with respiratory viral infections, especially in the exacerbative stage. In relation to definition, epidemiology, and pathophysiology, this review aims to summarize current knowledge concerning exacerbation of both COPD and asthma by focusing on the clinical significance of associated respiratory virus infections. PMID: 24098299

Prevention

RSV is spread by what is called ‘shedding’ – coughing and nasal secretions:

Children with respiratory syncytial virus (RSV) infection shed virus for variable periods. The aim of this study was to quantify the viral load in nasopharyngeal aspirates of children with RSV throughout their hospitalization. This study included 37 children who were admitted with a diagnosis of RSV infection based on a positive rapid diagnostic test. Nasopharyngeal aspirates were collected from patients every day, from admission to discharge….. patients shed detectable virus from days 1 to 12…. Half of the RSV-A patients were also positive on day 14 following onset. ……. Because RSV shedding was frequently prolonged, the hospitalized children may have contracted RSV as a nosocomial infection. To prevent nosocomial RSV infections in hospital wards, healthcare workers must take appropriate infection control measures and provide adequate guidance on hand washing to the family of the patient.  PMID:  26588816

In other words isolation and rigorous hygiene should be used, if RSV is detected.

Diagnosis

 

There are tests that can identify the virus

Respiratory samples (n = 267) from hospitalized patients with respiratory symptoms were tested by real-time PCR, viral culture, and direct immunofluorescence for respiratory syncytial virus, influenza virus, parainfluenza viruses, and adenoviruses. Compared with conventional diagnostic tests, real-time PCR increased the diagnostic yields for these viruses from 24% to 43% and from 3.5% to 36% for children and adults, respectively.  PMID:  17507513

Treatment

Symptom based medicine - Conventional medicine is somewhat at a loss to help as it says on Wikipedia “A prophylactic medication (not a vaccine) exists for preterm (under 35 weeks gestation) infants, infants with certain congenital heart defects (CHD) or bronchopulmonary dysplasia (BPD), and infants with congenital malformations of the airway. Treatment, however, is generally limited to supportive care (e.g. C-PAP), including oxygen therapy.”

Cause based medicine - Dr Duke’s list of plants that have AntiRSV activity is provided as an observation.  Again according to his analysis there is only one Chemical with Antirsv Activity and that is  ANAGYRINE.

This virus appears not to like heat.  It appears during the winter when we get cold and in the rainy season, when people of warmer climates get cold.  In temperate climates there is an annual epidemic during the winter months. In tropical climates, infection is most common during the rainy season. These are times of low immunity - cold stresses the immune system.   Thus the answer would seem to be a mixture of preventative medicine – always stay warm and well wrapped up – and to possibly use hot baths and saunas.

The main protection we have against this virus is our immune system and thus we need to boost the immune system with good healing food, warmth, and plenty of rest and relaxation.  Furthermore any form of compromising of the immune system by drugs such as immunosuppressants is madness and to be avoided at all costs. 

We identified 59 patients with a median age of 5 years; …. 39% had received corticosteroids, and 76% cytotoxic chemotherapy within 1 month before RSV infection.  PMID: 24327130

Oncolytic activity

 

This final section is perhaps one of the most interesting and key.  RSV is an oncolytic virus.  An oncolytic virus is a virus that preferentially infects and kills cancer cells.  As the infected cancer cells are destroyed by lysis, they release new infectious virus particles to help destroy the remaining tumour.  Oncolytic viruses are thought not only to cause direct destruction of the tumour cells, but also to stimulate host anti-tumour immune responses.  And from early evidence it appears that RSV is an oncolytic virus:

In several reports, the respiratory syncytial virus (RSV) was identified as an oncolytic virus in cancer cells (e.g., lung and prostate cancer). However, the effects of RSV in hepatocellular carcinoma (HCC) cells have not yet been investigated. Here, we observed the inhibitory effects of RSV infection in HCC cell-lines. Cell growth was significantly decreased by RSV infection in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. After RSV infection, plaque formation and syncytial formation were observed in affected Hep3B and Huh-7 cells. RSV protein-expression was also detected in Hep3B and Huh-7 cells; however, only Huh-7 cells showed apoptosis after RSV infection. Furthermore, inhibition of cell migration by RSV infection was observed in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. Therefore, further investigation is required to clarify the molecular mechanism of RSV-mediated inhibition of HCC cell growth.  PMID:  25739391

And

Oncolytic virotherapy is an emerging biotherapeutic platform for cancer treatment, which is based on selective infection/killing of cancer cells by viruses. Herein we identify the human respiratory syncytial virus (RSV) as an oncolytic virus. Using prostate cancer models, we show dramatic enhancement of RSV infectivity in vitro in the androgen-independent, highly metastatic PC-3 human prostate cancer cells compared to the non-tumorigenic RWPE-1 human prostate cells. The oncolytic efficiency of RSV was established in vivo using human prostate tumor xenografts in nude mice. Intratumoral and intraperitoneal injections of RSV led to a significant regression of prostate tumors. Furthermore, enhanced viral burden in PC-3 cells led to selective destruction of PC-3 cancer cells in vitro and in xenograft tumors in vivo due to apoptosis triggered by the downregulation of nuclear factor-kappaB (NF-kappaB) activity (and the resulting loss of anti-apoptotic function of NF-kappaB) in RSV-infected PC-3 cells. The intrinsic (mitochondrial) pathway constitutes the major apoptotic pathway; however, the death-receptor-dependent extrinsic pathway, mediated by the paracrine/autocrine action of tumor necrosis factor-alpha produced from infected cells, also partly contributed to apoptosis. Thus, the oncolytic property of RSV can potentially be exploited to develop targeted therapeutics for the clinical management of prostate tumors.  PMID:  19444304

This puts this virus in a different light.  If we now review all the evidence above, is it possible that RSV emerges when we are being attacked by other viruses which have not been identified?  Are the symptoms only those of a side effect of battle - a virus battle in our bodies.  Many children are born with viral infection obtained from their mothers, does the RSV virus attack these viruses causing acute symptoms of battle?

In effect, is the virus a 'good' virus in the same way that we have 'good' bacteria? 

These questions and many more need to be answered before we use antivirals or use this virus in battles with cancer.

We will also leave you with one last thought.  The measles virus also shows signs of being an oncolytic virus.  Measles virus strains have shown "considerable oncolytic activity against a variety of solid tumers and hematologic malignancies".

 

References and further reading

  • Br J Exp Pathol. 1964 Dec;45:647-55.  SURVIVAL OF THE RESPIRATORY SYNCYTIAL VIRUS DURING STORAGE UNDER VARIOUS CONDITIONS.  HAMBLING MH. PMID: 14245166
  • Acta Paediatr. 2000 Jun;89(6):654-60.  Long-term effects of respiratory syncytial virus (RSV) bronchiolitis in infants and young children: a quantitative review. Kneyber MCJ1, Steyerberg EW, de Groot R, Moll HA.
  • Pediatr Int. 2015 Oct;57(5):1038-40. doi: 10.1111/ped.12785. Pneumomediastinum, pneumorrhachis and subcutaneous emphysema associated with viral infections: Report of three cases.  Emiralioğlu N1, Ozcan HN2, Oğuz B2, Yalçın E1, Doğru D1, Özçelik U1, Kiper N1.   1Department of Pediatric Pulmonology, Hacettepe University School of Medicine, Ankara, Turkey. 2Department of Pediatric Radiology, Hacettepe University School of Medicine, Ankara, Turkey
  • Front Microbiol. 2013 Oct 1;4:293. doi: 10.3389/fmicb.2013.00293.  Virus-induced exacerbations in asthma and COPD.  Kurai D1, Saraya T, Ishii H, Takizawa H.  1Department of Respiratory Medicine, Kyorin University School of Medicine Mitaka, Tokyo, Japan.
  • J Med Virol. 2015 Nov 20. doi: 10.1002/jmv.24434. [Epub ahead of print]  Respiratory syncytial virus shedding by children hospitalized with lower respiratory tract infection.  Takeyama A1,2, Hashimoto K2, Sato M2, Kawashima R1, Kawasaki Y2, Hosoya M2.  1Department of Pediatrics, Soma General Hospital, Fukushima, Japan.  2Department of Pediatrics, Fukushima Medical University, School of Medicine, Fukushima, Japan
  • BMB Rep. 2015 Oct;48(10):565-70.  Effect of respiratory syncytial virus on the growth of hepatocellular carcinoma cell-lines.  Choi SH1, Park BK1, Lee KW2, Chang J3, Lee Y4, Kwon HJ5.
    • 1Departments of Microbiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
    • 2Departments of Biomedical Science, College of Natural Science, Hallym University, Chuncheon 24252, Korea.
    • 3Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul 03760, Korea.
    • 4Department of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju 28644, Korea.
    • 5Departments of Microbiology, College of Medicine, Hallym University, Chuncheon 24252; Center for Medical Science Research, College of Medicine, Hallym University, Chuncheon 24252, Korea
  • The Oncolytic Effect of Respiratory Syncytial Virus (RSV) in Human Skin Cancer Cell Line, A431. - Salimi V, Tavakoli-Yaraki M, Mahmoodi M, Shahabi S, Gharagozlou MJ, Shokri F, Mokhtari-Azad T.  Iran Red Crescent Med J. 2013 Jan;15(1):62-7. doi: 10.5812/ircmj.4722. Epub 2013 Jan 5.  PMID: 23487261
  • Oncolytic targeting of androgen-sensitive prostate tumor by the respiratory syncytial virus (RSV): consequences of deficient interferon-dependent antiviral defense. Echchgadda I, Chang TH, Sabbah A, Bakri I, Ikeno Y, Hubbard GB, Chatterjee B, Bose S. BMC Cancer. 2011 Jan 28;11:43. doi: 10.1186/1471-2407-11-43. PMID: 21276246
  • Anticancer oncolytic activity of respiratory syncytial virus. - Echchgadda I, Kota S, DeLa Cruz I, Sabbah A, Chang T, Harnack R, Mgbemena V, Chatterjee B, Bose S.  Cancer Gene Ther. 2009 Dec;16(12):923-35. doi: 10.1038/cgt.2009.34. Epub 2009 May 15. Erratum in: Cancer Gene Ther. 2009  Dec;16(12):936. PMID: 19444304

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