Re: Is there not a method of illuminating viral pathogens?

I think what you are asking is whether there is a way to make HIV more 
attractive to your innate immune system.  

When antibodies bind to a bacteria, (opsonization), it attracts 
macrophages and neutorphils to come over and gobble the little guy up.  
Immunizations containing antigens of bacteria capsules help immune 
response by inducing the production of antibodies for those pathogens.  

We have a problem with viruses, (cancers & mycobacteria), however, because 
these tiny “energy-less” basic life forms float around until they find a 
cell to hide in, insidiously subverting the cells genetic machinery for 
its own replication, thereby successfully hiding from antibodies and 
immune components.  When our cell host has successfully bred zillions of 
replicated viruses, the cell explodes releasing its sordid crew of viral 
parasites, each seeking new cells for continued viral production.  So what 
is there to do if the virus hides within our own cells?  A marker or 
antibody won’t do much good in that case!  Viruses that grow within the 
cytoplasm and the nucleus of an infected cell, can be eliminated only by 
killing their host cells!  

There is a special part of our immune system to detect intracellular 
parasites such as viruses, as well as cancerous cells.  This part of our 
immune system can inspect each of our own cells in an effort to determine 
if they are sick.  If its determined that one of our cells is “sick”, then 
our immune cell will gobble it up.  

A very important concept to understand here is the TH1/TH2 paradigm in 
immune function.  In the interest of brevity, I will say that the TH2, or 
humoral immune system is best at eradicating bacterial pathogens.  The 
TH1, or cellular immune system is better at detecting and eradicating 
viral and cancer infected cells.  

Its probably worth a brief overview of immune function at this point.  

Bone marrow stem cells will differentiate into red blood cells, 
macrophages, phagocytes (mononuclear phagocytes, neutrophils, 
eosinophils), auxiliary cells (basophils, mast cells, platelets), and 
lymphocytes.  Lymphocytes will further differentiate into the B-cell line 
and the T-cell line of cells.  B-cells will create Plasma cells and memory 
B-cells.  The Plasma cells will later become antibodies.  The T-cell line 
will become T-helper cells, T-cytotoxic (killer) cells, and T-suppressor 
cells.  

The T-helper cells breakdown into several classes, the most important 
being TH1 (cellular), and TH2 (humoral) immunity.  TH2 humoral cells 
collaborate with B-cells for the production of antibodies, and thereby 
assist in bacterial infestation.  In cases of intracellular mycobacterial, 
cancer or viral infestation, TH1 cellular (cell-mediated) immunity turns 
to stimulate macrophages for pathogenic destruction.

Most immune responses involve both branches acting in concert.  There are 
some situations where the reaction is mutually exclusive.  Protection 
against extracellular infectious agents is mainly provide by TH2 mediated 
antibody response, (and subsequent opsonization) – Humoral Immunity.  
Protection against infectious agents living within the cells (where they 
cannot be challenged by antibodies) is mainly due to TH1 mediated 
macrophage response.  

Molecular biologist have recently discovered a so-called Th1/Th2 paradigm 
in disease states.  It would appear that based upon genetic and 
environmental factors, T cell clones in vivo immune responses show a 
dramatic Th1 or Th2 polarization.  This presents a problem when virally 
infected patients present with primary Th2 responses to infection.  
Several studies have elucidated that Th2-dominated responses favor HIV 
replication and disease progression , , , .  Moreover, Th1 clones have 
been shown to inhibit HIV replication in other HIV-infected cells .  

Since we know that Th1 implementation and Th2 deactivation assists in HIV 
eradication, the issue now becomes how to accomplish this task.  

Th2 cells produce the cytokines IL-4, IL-5, IL-6, IL-9, IL-10 and IL-13 
and provide optimal help for humoral immune responses including the 
antibodies IgE, IgA and IgG, as well as the production of mast cell and 
eosinophil growth.  Through experimentation, IL-12 and/or anti-IL-4 
antibodies stimulate Th1 predominance.  Understanding the ability to 
switch Th mode predominance under the Th1/Th2 paradigm has now led to some 
novel immunotherapeutic strategies.  

It has specifically been shown that some Th2 mediated cytokines upregulate 
HIV replication while Th1 mediated cytokines are inhibitory to HIV 
replication.  For example, IL-4 and IL-10 inhibit the ability of cytotoxic 
CD8 + cells to suppress HIV replication .  While Th1 cytokines IFN-alpha 
and IL-12 inhibit HIV replication .  Its also interesting that Th2 
cytokines IL-4 and IL-10 lead to mass lymphocyte apoptosis and thereby a 
major contributor to the depletion of CD4 T cells in HIV infected 
patients , , and the accelerated apoptosis of killer CD8+ T cells , .  

In studying the immunopathogenesis of HIV infection, defective production 
of IL-12 and IFN-alpha, together with the enhanced production of IL-10 by 
HIV-infected macrophages hamper the development of Th1 responses and favor 
Th2-like cell production further exasperating disease progression.

In summary, the immune system must find and then eradicate pathogens.  A 
virus is insidious, hiding within cells and subverting their genetic 
machinery for their own replication.  Thus Th2 mediated antibodies are 
unable to find these parasites; therefore another part of the immune 
system, the Th1 cellular (cell-mediated) system has been set aside to 
undergo the function of eradicating intracellular pathogens.  In the case 
of HIV, as well as Lupus, MS, RA, Chronic Fatigue Syndrome, Fibromyalgia, 
chemical hypersensitivities, Sarcoidosis, Hepatitis, (aging), et. Al., Th1 
cellular immunity is often mistakenly compromised while favoring a 
frustrated Th2 humoral response.  As a result, the viral disease 
progresses with ferocity.  

The idea here is to TURN-UP Th1 responses by the use of IL-12 and IFN-
alpha in an effort to accelerate cellular immunity.  By doing this we are 
able to help the immune system find and fight these little monsters.  [As 
Th1 responses go up, Th2 responses abate].  

In final note:  There is no panacea in the treatment of chronic illness, 
whether it is diabetes, aging or HIV.  It takes rather a plethora of 
strategies to contain disease progression.  To date, we can completely 
contain disease progression for life in HIV infected individuals, but the 
financial cost and effort is incomprehensible.  To completely eradicate 
the disease, I would suggest that the patient undergo the myriad of known 
successful strategies – But add to it the novel immunotherapeutic 
application of Th1 cellular immunity stimulates.  

 1 Romagnani S, Maggi E, Del Prete G-F et al.  Role for Th1/Th2 cytokines 
in HIV infection.  Immunol. Rev. 1994; 140:73-92.
 2 Isreal-Biet D, Labrousse F, Tourani J-M, Sors H, Andrieu J-M, Even P. 
Elevation of IgE in HIV-infected subjects: a marker of poor prognosis.  J. 
Allergy Clin. Immunol. 1992; 89:68-75.
 3 Vigano A, Principi N, Crupi L, Onorato J, Vincenzo ZG, Salvaggio A. 
Elevation of IgE in HIV-infected children and its correlation with the 
progression of disease.  J. Allergy Clin. Immunol.  1995; 95:627-632.
 4 Bentwich Z, Kalinkovic A, Weisman Z.  Immune activation is a dominant 
factor in the pathogenesis of African AIDS.  Immunol. Today 1995; 16:187-
191.
 5 Vyakarnam A. Mechanisms for an opposite role for Th1/Th2 cells in 
AIDS.  Res. Immunol. 1994; 145:618-624.
 6 Barker E, Mackewicz CE, Levy JA.  Effects of Th1 and Th2 cytokines on 
CD8+ cell response against HIV: implications for long-term survival.  
Proc. Natl. Acad. Sci.  USA 1995; 92:11135-11139.
 7 Poli G, Fauci AS.  The effect of cytokines and pharmacologic agents on 
chronic HV infetion.  AIDS Res.  Human Retrov. 1992; 8:191-197.
 8 Groux H, Torpier G, Monthe D, Mounton Y, Capron A, Ameisen JC.  
Activation-induced death by apoptosis in CD4+ T cells from HIV-infected 
asymptomatic individuals.  J. Exp. Med.  1992; 175:331-340.
 9 Meyaard L, Otto SA, Jonkeer RR, Mijnster MJ, Keet RPM, Miedema F.  
Programmed death of T cells in HIV-1 infection.  Science 1992; 257:217-219.
 10 Lewis DE, Ng Tang DS, Adu-Oppong A, Schober W, Rodgers JR.  Anergy and 
apoptosis in CD8+ T cells from HIV-infected persons.  J Immunol. 1994; 
153:412-420.
 11 Meyaard L, Otto SA, Keet IPM, Roos MTL, Miedema F.  Programmed death 
of T cells in HIV infection.  J. Clin. Invest.  1994; 93:982-988.