By Adewusi B. Olusegun MB;BS(Ib) , Mchir;MD(Oxon)
(c) 2009
SUPPOSITION
According to Berkovich: “Basically, two circumstances are surprising: how agents that do not replicate can affect growing cell populations and why a severe damage comes with particular conformational variations. An explanation can be given using the suggested barcode interpretation of the DNA.
Proteins harbored inside a cell are not involved in the transmission of the cell control information, but they can influence this process indirectly by modulating conformational oscillations of the DNA. In the case of gene substitution, the disruption in cell communications happens because cells use a wrong "barcode" key, in the case of an extraneous intervention, cell communications are performed with a right "barcode" key but are restrained by conformational influences of contaminating proteins.
The disruption of cell communications by external agents depends on the kinetics of the interplay between the processes of growth and contamination. Slowly dividing neural cells are more sensitive to the intervention of non-genetic materials as shown by the following simplified model.
Suppose that cell contamination is going at a constant speed and takes time – TP to reach the critical level; suppose that cell divisions occur at a steady rate with time interval between cell divisions being TD. Let pn present relative levels of cell contamination after nth division (n = 0, 1, 2…).
Since non-genetic materials do not replicate, as a result of cell division the level of contamination halves. This can be described by a recurrence equation with an initial value p0 = 0:
pn = pn-1 / 2 + TD / TP (1)
The solution of this equation is given by a geometric series which for sufficiently large n approaches 2× (TD / TP). The contamination process can reach the critical level, pn approaching 1,
Only if:
TD > TP / 2 (2)
This means that the destruction of cells under steady contamination by non-genetic material can occur when the time between cell divisions, TD, is sufficiently large. So, this destruction can happen for slow-dividing cells, like neural cells, but not for fast-dividing cells. This conclusion supports the idea suggested in that a similar prion type contamination may be also responsible for some neurodegenerative diseases where pathogenic agents are difficult to identify”. [84]
According to Sir Isaac Newton and he was very much corroborated by Albert Einstein; force is of absolute relevance when issues of constrain are to be argued.
Apparently this relativity can be expressed as follows:
Fa = F (-v)
Thus the absolute relativity of special exposure
Consequently such co-existence would have the following implication.
Fa – Fv = [Fma]0
Hence a pseudo neutrality of matter within a finite space as corroborated by the reports of Kimura which I had tagged culture shock.
Thus if:
E = Energy reserves
G = Galleria (as in culture shock)
R = Rationale (as in gradient attained)
I = Co-efficient of interdependency
Then:
E – G = [R]i
Hence the absolute relativity regardless of time constraint!
Consequently:
E – G = Hidden potential
Protease – inhibitors
The assertions above raise four cogent questions:
1. What does it mean really to have “HIV”?
2. How really is “HIV” originated?
3. What does it mean to have an innate resistance to HIV?
4. And what does it infer if it is missing?
This also traces out a directional pattern of overcome regardless of time constrain:
1. HIV infects personae
2. T-cell attacks HIV
3. Insufficient potency is triggered for T-cells
4. [T-cell]3 → [T-cell]0
5. Insufficiency and retro-emotional engagement forces retro-transposition and causes [T-cell]0.5
6. HIV infects T-cells
7. Checks this trends for host to continue growth:
[gene]3 → [gene]2 + [gene]1
+
[gene]3 ← [gene]0 + [gene]1 ↓
[gene]2
↓
[gene]3 + [gene]0
8. HIV is a miscopy of a DNA virus (PAPOVIRUS)
9. HIV is an unstable state and under critical conditions try to regain its more realistic DNA status
10. It doesn’t infect cells as a negative attack; rather it uses innate resources of host under critical environmental conditions to continue growth
11. This implies a case of an impossible gradient attained for a compromised human immune defense system
12. Thus the virus HIV self triggers itself to attain stability; independent of host but as a result of a requisite environment and a possibility remnant T-cell pseudo gene that has documented a lost heritage for the virus
13. Acquired immune deficiency syndrome is a toxicity effect of this growth trend being altered; and it can only be experienced by a person with a resident retro-lifestyle
Theoretically then it might be possible to utilize a certain substance-x to isolate single strands from the retrovirus (RNA) in a new type of reaction to generate “allergically” recognizable and destructible proteins in the form of x-DNA.
Substance-X + Single strand retrovirus (RNA)
↓
Allergically destructible X-DNA
Thus creating the following possibilities:
1. Overcome cDNA excess in infected individuals
2. Substance-X to be used to neutralize RNA strands by combining with it to form X-DNA
3. Substance-X to be synthesized using Hybridoma technology
4. But it would still remain the human retro-status regardless of HIV
5. It would seem that there is a perpetual gradient appeal for HIV to stabilize as a retro-DNA
PRO-ACTIVITY
Another issue probably why a vaccine approach has not been successful is the issue of a damaged emotion override network which includes the limbic system and hypothalamus et al; [76] thus a definitive complex irrationality.
Moreover the ideology of a true vaccine for induced resistance to infection is based solely on the “emotion override – memory system” which in the case of HIV/AIDS are declared to have become dysfunctional. [95]
So the apparent questions then are:
1. How could the morphological defects induced non-functionality of the emotion override systems be cured?
2. Is it present in all cases that graduated to syndrome status?
3. Is it present in all cases reviewed?
4. Will a synthetic compound DNA-X still be recognized by an immune system that has; so to speak become invalidated and dysfunctional?
5. How is the associatable immunity disorder in all graduated cases [94, 95, 96] to be cured; inclusive of the damaged emotional networks?
6. Does the present array of psychotropic drugs target the failed immune system and failed emotional networks and other associated memory function?
Consider the illustration below:
Emotion Override = Cognition + Association – Sympathetic response (restrain)
That is:
[Rationale]i = Hidden Reserves – [Galleria]0
Hence an implied fringe behaviour defect in syndrome cases descriptive as self attack for HIV graduated symptoms; in other words sympathetic response decline experienced as a non nullity function for real culture shock episodes.
As such:
Resolve
(Independent Case) (Independent Case)
* Co-habitation not required; in other words each exists without the other’s after-resolve
Traumatic
Environment
Critical
Condition
Trauma
Human Rationale Cultured
* Trauma; based on history with an erstwhile environment
So two basic issues stand out; and these are:
1. Normalisation of environment engaged choice rationale
2. Reality of such environment induced compensation
Thus such pathogenic normalisation eventually causes trauma in the affected entity howbeit independent, but pathogenic compensation is expressed only in cases of an inflammatory response.
Inasmuch as the sympathetic and other co-dependent systems are fully functional then issues of inflammatory response are usually resolved by the body shock absorber networks but the consequent excess shock lagged to trauma is only due to such allergy storage as an accepted reality beyond acceptable stretches.
Hence creative parameters that either fixes trauma or its preemptive environment though with perpetual constraints of:
• Time
• Gradient
• Energy
Consequently we can implicate time for shock lapsed to trauma, gradient for inflammation to be recognized, and energy for fixing fringe resolutions.
If these constraints are to be properly implicated and isolated for further investigative protocols; then there must be routine procedures to compliment the present detection or examination techniques.
Unfortunately when Kimura and co. were involved in extensive examination of molecular data and its evolutionary trends there were not enough appraisals method that could isolate beyond separation of composite entities. [7, 8, 16, 17, 18, 19] Hence the need to distinguish the quality of contribution of certain distinguishable fringe resolutions.
And they can be resolved as:
1. Cognizance for furtherance or genetic preparedness
2. Definitive lifestyles consequence registered molecularly
3. Psychotropic interactivities with realistic environments
4. Morphology defects due to unrealistic environment
Thus with these new statutes it will now be possible to implicate amongst all other issues already available, the following critical environmental conditions for a pathological antigen – antibody reactions.
PH → Gradient
Temperature → Energy
Equivalence Zone curve → Time constraints
BRAIN ALLERGY – FRENZY
There is a PROZONE phenomenon where antibody apparently reacts more strongly at higher dilutions while failing to react at a lower dilution (higher concentration). It is due to a lack of an optimal proportion between antigen and antibody.
It is important to consider the prozone phenomenon when antigen – antibody reactions are used in the diagnosis of human diseases to avoid false negative results, especially when using qualitative techniques such as:
• Slide agglutination tests with the precipitin curve
Thus if there is a prozone phenomenon then there is a real antigen – antibody relative complexity worth further immunology investigation; in other words an implied choice rationale. [21, 22, 23]
In exaggerated Psychotropism that is implicated in retro-lifestyles; choice rationale when expressed as % fractionate value is always greater than 100% realistically. Thus granting statutory cases of would be juxtaposition exposures and further warranting issues bordering on:
1. Certainty
2. Reality
3. Specificity
But scores below 50% would only warrant composite investigation techniques as in the cases of supposition and override surge implications. This implies constraints that might have been both fixed and dynamic, thus its relative potentiality as a co-dependency fractionates value derived by comparative analysis of factual data and its matter substantiate counterpart.
Hence choice rationale for a given event or occurrence can be in truth a real constraints for propagation or extension for other but differing independent probable co-opts.
e.g.
Action/Impact = 4/5 = 0.8 = 80%
Other; 1/5 = 0.2 = 20%
Hence function 0.8 is a fixed constraint to function 0.2 if under considerable parameters it is always true. But if it changes depending on the parameters then it is still a constraint but a dynamic one that would require normalisation.
As such constraints or rationale can be further normalized as follows:
Certainty:
When an antigen reacts with its corresponding antibody, they form antigen – antibody complex often referred to as immune complex. Non covalent binding forces are involved in antigen – antibody combinations; therefore the antigenic determinant must have close proximity before the reaction can occur.
Specificity:
Such molecular unions are specific and as such an antigen will only react with its corresponding antibody and with no other. This behavior is governed by:
1. Presence of determinant groups on the antigen
2. Type of amino acids present in the antigen – binding region of Immunoglobulins
3. Pattern of amino acids present in the antigen – binding region of Immunoglobulins
Reality:
Many factors are responsible for the environment that creates an antigen – antibody complex; this includes:
1. Physiological range of PH is required for a firm union i.e. (7.2 – 8.2). At acidic PH range (3.0 – 4.0) the union of the complex breaks down.
2. Also the optimal temperature for an antigen – antibody reaction depends on the type of antibody. E.g.
(Cold agglutinin) IgM → 4˚C
(Warm antibody) IgG → 37˚C
3. There is also an optimum concentration (or equivalence zone) where antigen – antibody reactions occur.
For further macro causative rationale these could also be compared:
1. Weight/Age
2. Blood pressure
3. Height/Age
4. Waist size/Age
5. Adrenaline and Kidney statutes
Thus if rationale is plotted against constraints; including time relative constraints then the results should be a BRAIN ALLERGY COMPENSATION CURVE as illustrated below.
* Brain Allergy Compensation Curve
Thus a real compensation only occur prior or post initial frenzy; though occurrence post frenzy is a most technical/radical possibility.
It would require specificity, certainty, and reality of gradient achieved within initial frenzy and the constraint that supposedly prevented the attainment of an assumable “REAL” target.
Hence an emotion override onwards terminal compensation or newer latency statutes to requisite frenzy heights and eventual termination or perpetual emotion override compensation.
As such as reported by Gojobori “It is known that although the rate of amino acid substitution for a given protein is roughly constant over species, the rate varies considerably from protein to protein…. The functional constraint of proteins is also expected to affect the level of genetic variability in populations. In the last decade many authors have attempted to establish the relationship between protein function and genetic variability in populations……Johnson classified enzymes into three groups
• Variable substrate enzymes
• Regulatory enzymes
• Non regulatory enzymes
Examining the available data on protein polymorphism, he concluded that the first group has the highest average heterozygosity whereas the third group has the lowest….. He also pointed out that substrate – specific enzymes have lower variances than the expected values…… Except Yamazaki’s study, however, these studies were mainly concerned with the possibility of the existence of balancing selection in heterogeneous environments rather than the functional constraints of proteins……… If a protein has a strong functional constraint, many mutational changes in the protein are expected to be damaging to the protein function……….. This suggests that if sufficient data are available, the presence of functional constraints can be detected by studying the relationship between the mean and variance of heterozygosity. [8]
Thus a graph of mean vs. variance would produce a fixating gradient per investigated personae/entity; and as such become its functional constraint howbeit for the supposed instance, thus eliminating furtherance dynamism and engaging a yet to be deciphered equilibrium theory of population genetics.
Subsequently it would be requisite to focus on:
• Duplicate gene expression
• Pseudo genes
• Fixation of null alleles
• Loss of duplicate gene expression
• Iso-enzyme techniques on mitochondria DNA
Other macro implications would include:
• Vagus nerve consequences on the nucleus accumbens
• Gastro-intestinal pH and its relativity to septicemia
• Heart rate and its relativity to insufficient perfusion
• Frigidity/sex bruises and its maximum impact linkage for viral protein
• Biofeedback function of mitochondria DNA damage and pseudo genes proliferation
It would also be requisite to be able to image study direct effects of vagus nerve stimulation on the emotion override networks of the brain. And if there can be any plastic resuscitation of failed vital neural complexes.
The precursor cells of the immune system develop early in intra-uterine life, thus the need for theoretical variables linkage for both retro-lifestyles and HIV; moreover since all cell types participating in immune responses originate from the bone marrow as pluripotential stem cells and then become self perpetuating; multipotent and differentiated. Definitely the main reason why bone marrow transplants have not been successful in all cases it had been surgically applied to. [24, 25, 40, 71]
LINKAGE DISEQUILIBRIA
Kimura reported; “several years ago, the possibility of marked non – random association of polymorphic variants between different gene loci on one chromosome (called “linkage disequilibrium”) was suggested based on simulation experiments assuming balancing selection ………… It is assumed that the entire space of allelic states can be represented by integers on the horizontal axis, and that whenever a mutation occurs to a gene, its allelic states moves either one step in the positive direction or one step in the negative direction.” [5]
T. Mukai et al. further corroborated this unique postulation; “although the finding of Franklin and Lewontin described above was confirmed analytically by Slatkin, his results together with the findings of Yamazaki indicates that if the population size increases the formation of linkage disequilibrium becomes gradually more difficult or that the intensity of linkage disequilibrium decreases with an increase in the size of the population.” [7]
And I would assert this could only be as a result of extreme accumulation of null alleles thus creating an environment predominated by a juxtaposed null consequence functions and as such an onset negative directional trends as recorded in observed cases where supposedly fixed pseudo genes became unfixed null alleles. [10] And this more than any other assumption is what I would submit as the scenario that is been tackled as resultant complexes of the AIDS syndrome and retro lifestyles.
Scientific demographics and statistics available about lifestyles in Africa show a gloomy trend.
• 44% of Africans live below poverty line
• 33 out of the 41 heavily indebted poor countries are in Africa
• By 1996 Africa debt amounted to 64 billion dollars
• Africa economic growth: 1999 → 3.3%
1997 → 2.9%
Annual growth → 2.8%
• World growth 1998 → 2.0%
1997 → 4.0%
Despite African growth being higher than average world growth, the African growth is not high enough to make a real change for the people to reduce poverty. If Africa wants to reduce poverty by half over the next 15 years, it needs to attain and sustain an annual growth of 7%. Only North and Central Africa sub – Sahara regions grew in 1998. There were declines in the Eastern and Western sub – Sahara, including Nigeria; South Africa was basically unchanged, though it is well within expectations for these regions of stunted or retro-economic growth are the most implicated regions for the virus HIV. [46, 47, 48, 49, 50, 51, 53, 69]
As such it becomes pertinent to be wary of retro-engaging environments as much as it is necessary to find terminal resolutions for retro-episodes within the most reasonable time range.
A cross sectional study involving one hundred and eleven male prisoners was carried out by collecting data using an interviewer’s administered questionnaire in Nigeria on their perspective of what a risky behaviour is all about and its consequences.
• Knowledge of HIV/AIDS had affected the sexual practices of 100 (90.1%) inmates mainly in the areas of mutual fidelity to their partners (45.9%), and condom use (22.5%).
• Homosexuality (76%) was submitted as the commonest sexual practice in the prison.
• Seventy nine inmates (71.2%) had no idea as to the cause of HIV while twenty one (18.9%) affirmed of pre-information of a viral origin.
• Age range was 19 – 73yrs (mean = 32.5 +/- 11.0)
• About 50.5% were in the age group 20 – 30yrs
• About (45.9%) had been married before incarceration – * note that there is no gay marriage law in Nigeria
• Family and friends (31.5%), health workers (27%) and the mass media (26.1%) were their sources of information
• HIV prevalence in the prisons is usually higher than in the population at large; it could be as much as 5x, 6x, or 10x
• The prisons in developing economies are usually overcrowded
The primary goal of HIV/AIDS education within the prison systems is to prevent the transmission of HIV. A number of factors were postulated as dependent on whether a person will change a risky behaviour that carries the risk of HIV infection. Apart from the need to differentiate between risky behaviors when cases of preventive therapy of HIV/AIDS come to the fore and inability to link sexual behaviour successfully; since it was obvious the sexual linkage grew rather than subsided as would have been expected in a closed or finite community, while the disease itself did not culminate at a terminal peak as was recorded by the population charts of Kimura and co. [8, 11, 43] There is also the social responsibility aspect that as been put aside here especially the wider community’s well elaborated dependence on positive relationships; sexual obligations and community experience; there is also the issue of fidelity and child birth as we have always known it.
As such the general behavioral trends and the resultant growth charts of the disease rather excuses sex infinitely than implicate it as it would have been expected in all cases documented. [40, 42, 43, 44, 45]
One of the major manifestations of HIV/AIDS is in oral conditions; there are several oral manifestations of the disease, and among these the most common ones are:
• Candidal infection
• Necrotizing gingivitis
• Oral hair leukoplakia
These conditions are recorded as routine culture shock lag trends and can even manifest before a confirmation of seropositivity; thus granting an angle of a vocational hazard or failed independent personal health to the issue of HIV consequences. [52, 54]
Furthermore there is need for proper trauma scoring and these are most requisite especially in closed communities, where most health care is just basic and long distances in between specialization posts. Trauma registries provide an extremely useful tool in hospital quality improvement program. Certain factors identify patients requiring in-depth audit; these includes:
• Length of stay in the emergency department
• Excessive time to obtain a head CT scan in patients with altered mental status
• Time to operation in hemodynamically unstable patients
This would further help identify patients with error in diagnosis, error in judgment, error in technique, or inappropriate care. [56, 57, 58]
Clinical signs which are fairly accurate in the stable patient are frequently unreliable in the critically injured patient. There is a strong linkage of cardiac output as determinant to both septic shock and Hypovolemic shock. As such I would most readily implicate it and its pathological ramifications than sex for an HIV after – effect hypothesis. Interestingly it is measured as the area under a thermo-dilution curve; a simile brain allergy compensation curve frenzy region.
Causes of sepsis have been traced to:
• Pneumonia
• Intra-abdominal or severe wound infections
• Missed injuries or tissue necrosis
Septic shock commonly manifests as a hyper-dynamic state with:
• High cardiac output, 10 – 15 L/Min (normal range, 5 – 8 L/Min)
• Increased oxygen consumption
• Reduced peripheral oxygen consumption
• Fever
• Hypothermia
• Tachycardia
• Cutaneous vasodilation
• Hemodynamic instability
Supportive management of the patient with septic shock can be achieved with norepinephrine or epinephrine to maintain blood pressure and tissue perfusion pending removal or definitive treatment of the septic focus. [62, 75]
Neurogenic
Shock
Trauma
Override
Sympathetic
Relapse
pH
Et al
Miscopy
Infection
Septic
Shock
Compound Sympathetic
Malnourishment/ Response Decline
Retro-lifestyles
* Theoretical variables on the causative focus of HIV/AIDS & RETRO-LIFESTYLES
Trauma has assumed a malignant epidemic status with 1.2 million deaths yearly worldwide; 90% of which occur in developing countries mainly due to uncoordinated or lack of organized trauma care. In fact many developing countries do not have an ambulance or emergency rescue system in place that involves toll free call lines and Para-medics who specialize in pre-hospital care. The 10% cases of mortality from developed counterparts, despite the higher incidence of trauma, are traceable to the organization of trauma care. [63]
In the UK, the organization of trauma services can be traced to the Liverpool surgeon, Robert Jones, who in 1888 organized general surgical services for 20,000 workers of the Manchester ship canal company. Elsewhere in Europe and the rest of the world, mortality from trauma was alarmingly unacceptable, prompting the American College of Surgeons’ publication in 1966 describing trauma as a neglected disease of modern times. [63, 66, 67, 68] It has been noted that trauma results in an overall immunosuppressive state that culminates in post traumatic sepsis. Why some patients develop serious post traumatic complications and others do not is not fully understood, but genetic predispositions is suspected to be responsible. In patients with neurogenic shock, thoracic spine injury above T6 can be suspected. MRI scans remain the important imaging technique to assess the extent of injury. More also early post-injury depression and post traumatic stress disorder occur in about 15% of multiply injured patients and do not correlate with the severity of initial injury. [64, 65]
INFECTION
Serum proteins or Gamma globulins were first recognized and designated as a distinct group of proteins in 1937 by the process of electrophoresis on normal and immune sera. They migrated most slowly towards toward the anode, in an electric field at pH 8.6 than did the other two groups of globulins (alpha and beta). It was later at the World Health Organization meeting in 1964; when additional knowledge accumulated with the discovery of immuno-electrophoresis showed that observed gamma globulin fractions of serum contained several distinct antibodies containing protein whose classification could no longer be satisfactorily measured by immunoelectro-phoretic movements and other physico-chemical techniques, and they were termed immunoglobulins. [26, 90]
The five major classes of immunoglobulins are IgG, IgA, IgM, IgD, and IgE; the specificity of each antibody depends upon a definite amino acid sequence in their variable regions, the genetic markers in the light and heavy chains are inherited in a strict Mendelian pattern. They are normally difficult to detect in cerebrospinal fluid (CSF), since they are held back by the choroid plexus and meningeal vessels however the level rise when there is meningeal inflammation or an actual leak of blood. Recurrent bacterial infections occur in patients deficient in one or more of the four subclasses of IgG. Hyperglobulinaemia and constant production of antibodies are common findings in autoimmune diseases. [26, 27, 33, 72]
Radioimmuno- precipitation assay of patient antibodies to LAV p25. Produced virus was
metabolically labelled with [35S]methionine (molecular size markers in kilodaltons). Patient samples; 1, 4, 6, 9, 10, 13, 15, and 16 are highly positive sera; (lanes 2, 5, 12) weakly positive sera; and (lanes 3, 7, 8, 11, and 14) negative sera. The main protein specifically precipitated is p25. [97]
In 1981 a new serious medical syndrome was described in California and New York. The report identified clusters of previously healthy young men who suffered from different life threatening medical conditions previously not seen in this population. A task force led by the Centers for Disease Control (CDC) was set up, and defined the disease as the “Acquired Immune Deficiency Syndrome” (AIDS). It established that the syndrome was new and that the number of cases increased rapidly. A huge epidemiological survey initiated by CDC in 1982 concluded that the AIDS syndrome had spread globally. A subset of the population at particular risk for this syndrome appeared to be homosexual males and intravenous drug users, but there were also some cases in heterosexuals, hemophiliacs and immigrants from Haiti. The immunodeficiency was associated with rapid elimination of CD4+ T cells and antigen presenting cells. The clinical AIDS spectrum was defined as repeated opportunistic infections, specific malignancies and autoimmune phenomena occurring in previously healthy adults with no history of inherited disorders. [97]
Even though every cell in the body has antigens on its cell membrane, the lymphocytes are able to distinguish self from non self so as to prevent auto-immunity. During differentiation and specialization of lymphoid stem cells in primary lymphoid organs, most of the cells that are capable of causing auto-immunity are deleted. Yet, the body contains large numbers of lymphocytes that are self reacting. [24, 33, 90]
Bone Marrow Lymphocyte Precursors
↓ ↓
B lymphocytes Thymus (T lymphocytes)
↓ ↓ ↓ ↓ ↓
Memory B cells Plasma cells ← Helper/inducer Cytotoxic Memory
↑ T cells T cells cells
↓ ↑ ↓
Antibodies (Immunoglobulins) ↑ Cellular Immunity
↓ ↑
Humoral Immunity ↑
Suppressor T cells
(Inhibitory effect)
* Adaptation of the development of the Immune system [90]
The immune response to essentially all protein antigens requires initial processing and presentation to T-cells by antigen presenting cells (APC). T-cells recognize foreign antigens only when they are first broken down to short peptides and displayed in association with Major Histocompatibility Complex (MHC) proteins on cell surfaces. The MHC in man is the human leukocyte antigen (HLA) complex. The HLA plays a very vital role in the success or failure of any organ transplants and are highly immunogenic. In the 1950’s people who had received multiple blood transfusions or who had been pregnant several times over had antibodies against leukocytes of other members of the population in their serum. [28, 29, 30] Hence HLA testing is an insufficient criterion, if at all to confirm a pathological status or disease infection success; rather it is a representation of a status quo that might have been waylaid if disease infection became successful. It is the body’s register of self from non-self and its functionality proves sanity rather than insanity at the molecular level. The influence of MHC on determinant selection stems from the fact that any given allelic form of an MHC protein is only able to bind only a finite range of peptides. [29]
Virus production was detected by reverse transcriptase (RT) enzyme activity in supernatants from cultured and activated lymphocytes obtained from a lymph node from a patient with lymphadenopathy. Supernatants from cell cultures were analyzed by RT activity that was found in T4+ but not T8+ lymphocytes. [97]
Barré-Sinoussi and Montagnier were described in their Nobel Prize wining works as having studied a pair of siblings with hemophilia B (treated with factor VIII).
One brother was healthy but the other had symptoms of AIDS (Kaposi’s sarcoma). A virus similar to an already identified lymphadenopathy associated virus (LAV) was isolated in both cases with a typical lentivirus D-type of morphology, with cylindrical conical core distinct from the large spherical cores of HTLV-I and HTLV-II. They called this virus immunodeficiency associated virus (IDAV-1 and IDAV-2, respectively). They also isolated virus from peripheral blood obtained from diseased patients and demonstrated that this virus had a cytopathic effect that could promote giant cell formation in cultured infected T lymphocytes. [38, 97]
Furthermore, antibodies to their new virus were detected in individuals at risk for AIDS as well as those with AIDS and AIDS-related conditions but not in patients with other diseases. Thus, within one year Barré-Sinoussi´s and Montagnier´s group had characterized a virus from pre-AIDS and AIDS cases that had the following unique properties:
1. A 90-130 nm sized retrovirus with cylindrical core (D type) of lentivirus type that targeted CD4+ T cells.
2. It showed cytopathic effects in T cells plus an extensive virus replication that led to cell free virus transmission.
3. It did not cause cell transformation and had a unique p24 protein and this clearly separated the LAV/IDAV virus from HTLV-I and –II.
The discovery was accepted by the research community and resulted in an explosion of scientific breakthroughs; Professor Robert Gallo’s group at NIH described the detection of a novel HTLV-like virus from a vast number of patients with AIDS or pre-AIDS in 1984. The virus shared some properties with HTLV-1 and HTLV-2 and was denoted HTLV-III; however, it showed considerable similarities with LAV-1. By using newly developed immunological reagents and techniques, antibodies against HTLV-III proteins were found in a majority of AIDS and pre-AIDS cases and in clusters of homosexual men. Professor Jay Levy’s group in San Francisco also identified a D-type retrovirus, of the lentivirus group, which was structurally related to LAV-1 and HTLV-III, from AIDS patients and patients with lymphadenopathy. The virus was denoted AIDS associated retroviruses (ARV). The American and French teams agreed later that LAV-1/IADV-1/HTLVIII and ARV was the same type of virus. An international virus taxonomy consortium chose in 1985 to name the virus Human Immunodeficiency Virus type 1, or HIV-1. The virus belongs to the lentivirus subfamily of retroviruses which is distinct from the previously identified human retroviruses, the oncogenic leukaemia viruses HTLV-I and II. Lentiviruses group contain viruses that cause persistent viremias in monkeys, cats, horses, cattle and sheep. Extensive seroepidemiological work by several research groups led by Robert Gallo, Luc Montagnier, Max Essex, William Haseltine, Jay Levy and Robin Weiss further confirmed the causative role of the virus in the development of acquired immunodeficiency syndrome, AIDS. [32, 35, 97]
It has since then been confirmed that once inside the body, the virus tend to target the helper T cells; the cell infected are ultimately killed thus reducing the number of helper T cells in the body. Since the suppressor T cells are not infected the immune system becomes depressed further thus making the body vulnerable to all types of infection. [90] Moreover the graph of viral activity above shows a compensatory curve like the brain allergy compensation curve and as such a negative prozone phenomenon which normally should have been missing in an howbeit override surge as is supposed to be present in a real virus infection success in other words a straight line graph as produced by Kimura and co. Hence I disagree that HIV-1 capacitates itself without an opportunistic environment and this environment I submit must be pathological for the co-infection to be realized; its activation is as a result of an opportunistic requirement and hence it does not cause opportunistic environment it has already become resident prior viral activation. The question left then is what is this environment?
Immune tolerance refers to a state of immunological unresponsiveness to a particular antigen and this is important in preventing autoimmunity to self antigens. Consequently immune tolerance is achieved by deletion of self reacting lymphocytes from peripheral repertoire (clonal deletion), thus preventing further differentiation of immature cells capable of self reacting (clonal abortion) or down regulation of response (clonal anergy). Immune tolerance is epitope specific and may be complete or partial. [34] Hence the purported HIV-1 accessory proteins ability to evade from various forms of cell mediated (or intrinsic) anti viral resistance can be taken for an immune tolerance of self howbeit partial. [99]
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