Maladaptive Responses to Immune Disorders

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Maladaptive Responses to Immune Disorders

Per Huether & McCance (2012) “coping is the process of managing stressful challenges that tax the individuals’ resources” (p.217). Coping may be adaptive or maladaptive. Maladaptive coping results in a change that ultimately yields adverse reactions (p.217). For this week’s discussion, HIV and psoriasis are reviewed. Also, maladaptive and physiological responses of the two disorders will be compared. Finally, genetic factors will be examined and determine its impact on the pathophysiology of each disorder.

HIV (human immunodeficiency virus)

HIV is a blood-borne pathogen that enters the body through transmission of contaminated blood products, needles or sexual contact with an infected host (Huether & McCance, 2012, p. 184). HIV is a retrovirus which carries RNA rather than DNA, by way of the first viral enzyme reverse transcriptase. This enzyme converts RNA into a double-stranded DNA. By the use of a second enzyme integrase, the new DNA is inserted into the cell and lies dormant. HIV infection becomes active in the cell when there is formation of virions and cell lysis occurs. Protease is needed to process proteins and maintain the structure of the cell over time. If the cell remains dormant, the genetic material may remain latent in the body for years. The primary surface receptor for HIV is gp120, which binds to CD4 molecules on the surface of T cells. Other co-receptors such as chemokine or CCR5 are target cells (p. 184).


Psoriasis is characterized as a chronic, relapsing, proliferative inflammatory disorder that affects the skin, scalp, and nails. Inflammatory cytokines such as interlukins and tumor necrosis factor-alpha from activated T cells cause lesions. Hyperproliferation and thickning occurs in the dermal and epidermal layers of the skin, yeilding alterations in kerotinocyte differentiation, expansion of the dermal vascalature, and inflammation due to the neutrophil and lymphocyte infiltration. The epidermis thickens and plaque forms when cells mature and keratinization is bypassed. Because of loosely cohesive keratin, lesions often have a silver appearance. Erythema occurs due to dilation of the capillaries and an increase in vascularization to accommodate increased cell metabolism. Although plaque psoriasis is the most common, there are other forms, for instance, guttate, inverse, erythrodermic, and pustular (Huether & McCance, 2012, p.1049)

Maladaptive and Physiological Comparison

            Both HIV and psoriasis present maladaptive response mechanisms that affect the host’s immune system. HIV begans to weaken the immune system when activated, but may lie dormant over time. Psoriasis has no effect on the immune system and may affect a person soon after birth (Hammer, and McPhee, 2014, p. 191). Physiological presentation occurs slowly in HIV and can be ruled out initially due to the present of other common illneses, such as pneumonia, the common, cold, fatigue or other opportunistic infections (p. 51). Both psoriasis and HIV produce lesions. Skin lesions from HIV are typically due to an infectious bacteria such as Herpes Simplex or Zoster (p.55).  In psoriasis the lesions produce erythema and become dry and scaly, but are not infectious. The progression of each disease is different. Psoriasis spreads rapidly, and symptoms often recur (p.191),  while HIV progresses over time.      


A study conducted by Lonnberg et al. (2013) found that heritability exists in monozygotic (MZ) and dyzygotic twins (DZ). Because MZ twins share all the same genes and DZ twins share atleast half of the same genes (p. 413) , findings indicate that “genetic heredity exists for psoriasis 66-90% of the time” (p.412). “There is also an increased incidence in relatives of the affected individuals” (Hammer & McPhee, 2014, p.191). Psoriasis is still not cosidered an exclusive genetic disorder because some individuals never develop lesions (p.191). There have ben studies conducted on the genetic factors related to HIV as well. C-C chemokine receptor 5 (CCR5) has been shown to be a co-receptor for the macrophage-tropic strains of HIV-1 (1,2). In the mid-1990’s, it was discovered that a mutant variant of this gene with a 32 bp deletion in homozygous form provides almost complete resistance to HIV (1,2), whereas the heterozygous form provides partial resistance and slower progression of AIDS. This mutation is highly prevalent in European populations with an average frequency of 10% but it is almost absent in African, American Indian, and East Asian populations (Bilogav et al., 2009, p.35). Newer research on this gene mutation is still being conducted.


Biloglav, Z., Zgaga, L., Smoljanović, M., Hayward, C., Polasek, O., Kolcić, I., & … Rudan, I. (2009). Historic, demographic, and genetic evidence for increased population frequencies of CCR5Delta32 mutation in Croatian Island isolates after lethal 15th century epidemics. Croatian Medical Journal, 50(1), 34-42. Retrieved from Walden Library Databases.

McPhee, S. J., & Hammer, G. D. (2010). Pathophysiology of disease: An introduction to clinical medicine (Laureate Education, Inc., custom ed.). New York, NY: McGraw-Hill Medical.

Lønnberg, A. S., Skov, L., Skytthe, A., Kyvik, K. O., Pedersen, O. B., & Thomsen, S. F. (2013). Heritability of psoriasis in a large twin sample. The British Journal Of Dermatology, 169(2), 412-416. doi:10.1111/bjd.12375

McPhee, S. J., & Hammer, G. D. (2010). Pathophysiology of disease: An introduction to clinical medicine (Laureate Education, Inc., custom ed.). New York, NY: McGraw-Hill Medical.