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Sintomatologia – Tipicamente, a proctite causa um sangramento indolor ou a eliminacao de muco atraves do reto. Diagnostico – Para estabelecer o diagnostico, o medico proctologista examina o interior do reto com o auxilio de um proctoscopio ou de um sigmoidoscopio e coleta uma amostra de tecido do revestimento interno do reto para exame. Tratamento – No tratamento da proctite sao utilizados antibioticos, pois a proctite e causada por uma infeccao bacteriana especifica. Qualquer pessoa com um comprometimento do sistema imune tambem apresenta maior risco de proctite, especialmente devido a infeccoes causadas pelo virus do herpes simples ou pelo citomegalovirus. Paciente adolescente, compareceu ao consultorio, apresentando grave estomatite, de evolucao de 05 dias. Procedimentos: Ao exame objetivo da cavidade oral, apresentava Placa brancacenta saburrosa em toda a lingua, algumas exulceracoes, vesiculas e crostas sericas e hematicas Imagem A).
Houve completa involucao do quadro Estomatologico, voltando o paciente a ingerir alimentos normalmente. No retorno, o paciente trouxe os exames sorogicos solicitados, apresentando resultado da sorologia IgM para VHS com Titulo Positivo, confirmando nossa impressao diagnostica inicial. Quanto ao uso de Roacutan como desecadeante do quadro em apreco, achamos que nao tenha relacao como indutor; simples coincidencia. Herpes simples genital – E uma doenca causada por um virus que, apesar de nao ter cura, tem tratamento.
Formas de contagio – O herpes genital e transmitido por meio de relacao sexual (oral, anal ou vaginal) sem camisinha com uma pessoa infectada.
Sinais e sintomas – Essa doenca e caracterizada pelo surgimento de pequenas bolhas na regiao genital, que se rompem formando feridas e desaparecem espontaneamente. Tratamento – Na presenca de qualquer sinal ou sintoma dessa DST, e recomendado procurar um profissional de saude, para o diagnostico correto e indicacao do tratamento adequado.
Esses agupamentos de pequenas lesoes vesiculares associadas com intenso prurido e dor e caracteristico de infeccao pelo virus herpes simples. Embora as lesoes do virus do herpes simples tipos 1 e 2 possam ser indistinguiveis, a ausencia de fatores de risco para doencas sexualmente transmissiveis, faz do virus herpes simples tipo 1, adquirido como doenca ocupacional, o diagnostico mais provavel.
A disseminacao assintomatica dos virus do herpes e comum durante doencas graves, particularmente em pessoas imunodiprimidas. Nesse caso, deve-se distinguir paroniquia herpetica de infeccao bacteriana localizada, porque a tentativa de realizar drenagem das lesoes herpeticas somente prolongarao o curso da infeccao. As causas de celulite em trabalhadores da area de saude incluem bacterias rotineiras como, Staphylococcus aureus e estreptococos hemoliticos, e, mais raramente, Mycobacterium tuberculosis.
E muito importante a distincao entre as varias manifestacoes clinicas das infeccoes pelo virus herpes simples e pelo virus herpes zoster. Um aspecto caracteristico da infeccao pelo virus herpes simples e que, em seguida a infeccao primaria da pele ou membranas mucosas, os virus entram em um estado de latencia ou de adormecimento no interior das celulas nervosas nos ganglios.
As infeccoes recorrentes geralmente ocorrem na mesma area de pele anteriormente acometida, e precedida por formigamento, queimacao ou disestesias, seguidas pelo aparecimento de vesiculas agrupadas e pustulas. O herpes zoster e um doenca localizada caracterizada por uma dor radicular unilateral e uma erupcao vesicular que esta limitada a regiao do unico ganglio sensitivo espinhal ou craniano acometido (dermatomo). Um aspecto distintivo do herpes zoster e a localizacao e a distribuicao da erupcao, que geralmente e unilateral, nao cruza a linha media, e esta limitada a area da pele enervada por um unico ganglio sensitivo. Visitante, nos informe seu Perfil, para que possamos melhorar cada vez mais os assuntos do site.
Human Immunodeficiency Virus (HIV) is a lentivirus, a group of retroviruses, that causes slow development of acquired immunodeficiency syndrome (AIDS).
The innate immunity is the body’s first line of defense involving the skin and mucosal barriers as well as a nonspecific inflammatory response. The innate system cannot adapt to repeated exposure of a pathogen and does not distinguish between different invaders (non-specific).[4] Therefore, it responds the same way every time an antigen is encountered. Inflammatory mediators (mast cells, eosinophils, and basophils) and natural killer (NK) cellsare also involved in innate immunity.
This system complements the innate immune response by developing more specific responses in order to protect the organism from those pathogens that get past the innate cells. Antibodies present in the saliva, blood, or vaginal secretions mediate the humoral response and are very effective against foreign substances that can be easily reached and neutralized.
Like humoral immunity relies on B lymphocytes, cell-mediated immunity requires the function of T lymphocytes. Once a T cell interacts with a specific antigen, it produces a number of additional lymphocytes such as helper T cells (CD4+) and cytotoxic T cells (CD8+). In regards to the adaptive immune system, cytokines are responsible for proliferation and maturation of the lymphocytes that produce them. The immune system has a variety of responses based on the pathogen that is presented; therefore, it is difficult to define the typical response. Cytotoxic T cells (adaptive immunity) and NK cells (innate immunity) are activated and directly attack cells that have been mutated by a malignant process or virus.
The viral RNA encodes genes for proteins and enzymes essential to HIV replication and survival.
A protein that halts cell cycle and allows viral DNA to enter host cell nucleus in non-dividing cells (e.g. Any immune system or central nervous system (CNS) cells containing CD4 cell membrane receptors and the appropriate co-receptor on the plasma membrane. The CD4 molecule normally acts as a co-receptor of the major histocompatibility complex class II molecule for recognition of extracellular foreign bodies (antigens) by the T-cell.[1] When HIV binds to CD4, the gp120 alters its structure so that it can attach to the chemokine receptors on the cell membrane. Once at the surface of the nucleus, interaction of the PIC’s Vpr and integrase with various nuclear pore proteins allows entry into the nucleus.[12] The PIC is larger than nuclear pores.
Inside the nucleus, integrase controls attachment of the provirus’ 3’ hydroxyl groups (i.e. Inhibition of release of viral products appears to be controlled by the host cell transmembrane protein, tetherin. The innate and adaptive immune responses are both activated once HIV has infected the host, but they appear to be inadequate or too late to eradicate the virus.[4] The role of the adaptive immune response has been researched in greater detail as opposed to the more recent recognition and appreciation for the importance of the innate system in the pathogenesis of HIV. Once the virus has entered the host cells, the viral genome is transcribed and integrated with the host DNA and begins replicating many times[4], as described above.
Following the acute phase, the immune system responds strongly in order to decrease the viral load and increase the circulating CD4+ T cells; however, despite this attempt the host is not able to clear the infection[6].
Monocyte-Macrophage: The infection of the family of monocyte-macrophage cells by HIV-1 results in a persistant and chronic low-level infection.
HIV-1 infection and replication is highly regulated by cytokines produced by a variety of cells. Stimulates HIV-1 replication in peripheral blood mononuclear cells (PBMC), CD4+ T cells, and T cell lines. Mitochondria are often referred to as the power house of the cell, as it produces 90% of cellular ATP through the process of oxidative phosphorylation. Recent studies have primarily focused on the effects of HIV pharmacological interventions on mitochondria.
It has also been well documented that apoptosis is a primary mechanism responsible for CD4 T cell decline in HIV infected patients. The primary role of the Hypothalamic-Pituitary-Adrenal axis (HPA axis) is to maintain the basal and stress-related homeostasis of the central nervous system (CNS).
A high concentration of serum glucocorticoids has been shown to cause atrophy and dysfunction of the hippocampus.[36] The hippocampus, found in the medial temporal lobe of the brain, helps regulate the secretion of trophic hormones, such as corticotrophic releasing hormone (CRH), from the hypothalamus.
Furthermore, increased serum cortisol inhibits the production of cytokines, thus decreasing T-cell proliferation and function. As stated above, the adrenal androgen dehydroepiandosterone (DHEA) levels are often decreased in HIV-infected persons.


Association of HSP70 with a deaminating enzyme of the APOBEC family controls viral replication in the cytoplasm. Association of HSP70 with viral particles can be found extracellularly, particularly in blood serum.[40] Viral budding dissociates the cell plasma membrane from the host to envelope the new HIV virion. Opportunistic infections are highly likely in people with HIV.[4],[51] Examples of common infections can be found in Table 7. Folliculitis refers to the swelling or inflammation of one or more hair follicles that occurs on any part of the skin. Na proctite ulcerativa, uma forma comum de proctite, ocorre a formacao de ulceras no revestimento retal inflamado. Quando a causa e a blenorragia, o herpes simples ou o citomegalovirus, o anus e o reto podem ser intensamente dolorosos.
O laboratorio pode identificar bacterias, fungos ou virus que podem estar causando a proctite. Quando a doenca e causada pelo uso de um antibiotico que destroi as bacterias intestinais normais, o metronidazol ou a vancomicina deve destruir as bacterias nocivas que substituiram as normais. A cortisona, um tipo de corticosteroide, encontra-se disponivel sob a forma de uma espuma que pode ser introduzida no reto com o auxilio de uma seringa especial.
Paciente sem depressao imunologica, realizava tratamento de Acne e apresentava todos os exames complementares normais, inclusive sorologia para HIV e HTLV I e II. Alem disso, se apresentava com Febricula e Adenopatia sub-mandibular e estava com sua alimentacao prejudicada. Representa quadro alarmante e de sofrimento, impedindo o paciente de alimentar-se normalmente por periodo de 7 a 10 dias.
Seus sintomas sao geralmente pequenas bolhas agrupadas que se rompem e se transformam em feridas. Em mulheres, durante o parto, o virus pode ser transmitido para o bebe se a gestante apresentar lesoes por herpes. Antes do surgimento das bolhas, pode haver sintomas como formigamento, ardor e coceira no local, alem de febre e mal-estar.
O dedo polegar apresenta varias lesoes papulosas-vesiculares pequenas com eritema circundante.
A linfadenopatia e a linfangite sao inespecificas e pode ocorrer em qualquer tipo de infecao, e um sinal de defesa (limitacao do processo) e drenagem da area infectada. Ambas as infeccoes pelo virus herpes simples e pelo virus herpes zoster caracterizam-se pela presenca de multiplas vesisulas. Com a reativacao, o virus desloca-se para baixo ao longo da fibra nervosa para produzir a infeccao cutanea recorrente. Vesiculas e ulceras dolorosas ocorrem em areas mucocutaneas , como boca, faringe, cervix e genitalia externa; podem ser localizadas, mas encontram-se frequentemente disseminadas, envolvendo toda a boca ou areas extensas da genitalia. O HZ e resultante da reativacao do virus que se manteve em estado latente no interior do ganglio apos uma infeccao com varicela (catapora) que pode ter ocorrido na infancia. This results in immune system failure and increased suscepibility to life-threatening infections. The human body has typical physical barriers which protect us from pathogens including the gut, skin, urinary tract and mucous membranes of the bronchi. The innate immune system uses structures known as pattern recognition receptors (PRRs) to identify pathogens by a few evolutionary structures presented on large groups of microorganisms, termed pathogen-associated molecular patterns (PAMP)s.
Inflammation plays a key role in triggering an immune response that consists of a physiological cascade of events that responds to injury or infection. The adaptive immunity initiates a highly selective and specific response which becomes more effective on repeated exposure (memory). B lymphocytes (B cells) are coated in immunoglobulin, originate in the bone marrow, circulate in the extracellular fluid, and are responsible for producing the antibodies. Helper T cells recognize foreign antigens (synthesized outside the cell) bound to host proteins and aid the B cells to produce antibodies. When an antigen binds to a B or T cell, they produce cytokines which in turn begin proliferation of the B and T cells in the lymph nodes. Lentiviruses are a group of retroviruses, which means that they require the enzyme reverse transcriptase for transcription of its ribonucleic acid (RNA) encoded genes into DNA. After the initial binding to a host cell by viral gp120 surface receptor onto CD4, the virus must bind to a co-receptor to secure it to the host cell membrane.
Cytokine interactions can manipulate the genomic activation of integrated viral DNA in these cells. The CD4 T cells differentiate into effector T cells that activate their target cells through production of cytokines to help destroy pathogens [9].
Inhibition is associated with its ability to down-modulate production of IL-6 and TNF-?[21]. IL-4 induces NF-?B nuclear translocation stimulates HIV-1 replication in slowly maturing monocytes, but inhibits CCR5 expression and HIV-1 replication in young monocytes[21]. The chemiosmotic theory states the energy gained by respiration is converted into an electrochemical gradient across the inner mitochondrial membrane, which is thus used for ATP production. However, it has been shown that HIV directly affects mitochondrial function by impairment of complex 1 function of the electron transport chain. Both CD4+ and CD8+ T cells demonstrate a decrease in cell membrane potential, and subsequent apoptosis. When stimulated, a cascade of interactions is set off and any disruption has a significant impact on circulatory, behavioral, endocrine, immune, and cognitive functions.
Cytokines act as inflammatory signals and they are produced as a result of the innate and adaptive immune system activation. The primary purpose of CRH is to cause proopiomelanocortin (POMC) gene transcription to build the POMC peptide that allows formation of ACTH and other hormones.[36] The disruption in this mechanism results in further neuroendocrine dysfunction.
A study performed by Christeff and colleagues[37] found a negative correlation between CD4 cell count and cortisol concentration in individuals infected with HIV. HSP70 levels elevate in response to thermal changes in the cellular environment and with inflammatory or infection responses, such as with HIV.
The following is a table, classified by system, of the symptoms that have been commonly found in patients diagnosed with HIV. They are called “opportunistic infections” because the immune system is already functioning at a compromised level and unable to fight off infections that a healthy individual would otherwise be able to defend.
It begins where there is damage to the hair follicles through friction from shaving, clothing or blockage of the follicle. O medico tambem pode examinar outras areas do intestino utilizando um colonoscopio ou estudos radiograficos contrastados com bario. Concomitantemente, a sulfasalazina ou uma droga similar pode ser administrada pela via oral. Outras causas de proctite sao a radioterapia sobre o reto ou em suas adjacencias, Doenca de Crohn e colite ulcerativa. Na ocasiao, foi realizado a Impressao diagnostica de Gengivo-Estomatite Herpetica Aguda e solicitado sorologia de Imunoglobulinas IgG e IgM para VHS (virus do Herpes simples). Depois que a pessoa teve contato com o virus, os sintomas podem reaparecer dependendo de fatores como estresse, cansaco, esforco exagerado, febre, exposicao ao sol, traumatismo, uso prolongado de antibioticos e menstruacao.
Por ser muito contagiosa, a primeira orientacao dada a quem tem herpes e uma maior atencao aos cuidados de higiene: lavar bem as maos, evitar contato direto das bolhas e feridas com outras pessoas e nao furar as bolhas. Leves vergoes linfangiticos estao presentes em seu antebraco e forma palpados nodulos linfaticos epitrocleares e axilares.
The organism is protected from infection and disease when the immune system is working properly; however, failure of the system can result in infection or disease that is localized or systemic.
If the pathogen cannot be destroyed by the innate system alone, the adaptive immune system is mobilized.


Once the PRRs recognize a PAMP they activate a proinflammatory response that ultimately leads to production of cytokines, chemokines, and anti-viral type I interferon. An antibody is a receptor on each B cell that can recognize a specific antigen and immobilize it, thus preventing it from causing infection.
The precursors of T lymphocytes begin in the bone marrow but mature in the thymus where they learn to discriminate self from non-self. The CD4+ T cells also aid in the stimulation of the CD8+ T cells, through production of cytokines.
There is a 1000 fold expansion within 3-4 days of the responding cell allowing them to enter the circulatory system and be attracted to the site of infection by other cytokines and chemokines involved in the inflammatory response.[4] With repeated exposure to these antigens, the large population of B and T cells are maintained and are involved in the long-term memory for a more rapid response the next time the host is infected with that pathogen. The human immunodeficiency virus is spherically shaped with an outer phospholipid bilayer that surrounds the inner contents.[10] Multiple couplets of glycoproteins (gp 120 and gp41) are embedded over the outer surface of the virus and act as receptors for binding to host cell membrane receptors. A pharmaceutical against Nef may only interfere with one or two of its complex activities.[11] In vitro studies have discovered four key Nef functions that play possible roles in pathogenesis. Next, the extracellular portion of gp41 forms a loop structure that brings the virus and host cell membranes close to each other. The M-tropic (M indicates macrophage) strains of HIV-1 use the beta-chemokine receptor, CCR5, for cell entry into macrophages, CD4+ T-cells, and dendritic cells.
In other words, Tat takes over control of transcription from the host cell once NF-KB is bound to the LTR. Early synthesis and adequate accumulation of the viral protein, Rev, assists in the export of viral RNA from the nucleus.
Interleukin (IL)-2 is one type of cytokine secreted by an effector T cell that upregulates HIV-1 replication in certain cells but can also stimulate CD8+ T cells that result in suppression of HIV-1 replication in other cells.
Several studies have shown that HIV-1 infection results in HPA axis activation and abnormality.[32] There are proposed mechanisms to explain this phenomenon. The cytokines associated with HIV include tumor necrosis factor-alpha (TNF-?), interleukin (IL)-1 and IL-6.[32] They directly activate the hypothalamus. Severity, duration and time in which the symptoms appear in the course of HIV also vary among individuals infected with HIV. Constitutional symptoms including fever, sore throat, weight loss, lethargy, fatigue, and night sweats are common.[4] Other organs in the body are not immune to the effect of HIV. Alguns casos respondem prontamente ao tratamento, enquanto outros persistem ou recorrem, exigindo um tratamento prolongado. Quando esses tipos de terapia nao reduzem a inflamacao, a administracao de corticosteroides pela via oral pode ser util. Em homens e mulheres, os sintomas geralmente aparecem na regiao genital (penis, anus, vagina, colo do utero).
Due to the diversity of existing pathogens, the immune system has to respond in a variety of ways and the response depends on the type of antigen presented. The CD8+ T cells target and lyse virally infected cells by recognizing foreign antigens (synthesized within the cell) bound to host proteins.
The gp41 portion crossing the viral phosphoplipid bilayer anchors the receptor to the membrane while the gp120 portion lies at the extracellular end of the gp41 stem.
Integrase also modifies viral proteins into their useable form.[1] Other viral genes encode for various other viral proteins and factors for survival.
The T-tropic (T for T-cell) HIV strains successfully bind to the alpha-chemokine receptor, CXCR4, for entry into CD4+ T-cells and macrophages. Host ribosomes translate viral mRNA into viral proteins.1 HIV-1 protease, which was released into the cytoplasm earlier, cleaves translated strands to complete synthesis of gp120, gp 41, p24, p17, and other viral proteins. NF-?B is translocated into the nucleus and ultimately makes the HIV-1 LTR more accessible and results in viral transcription. Specifically, mitochondria initiate apoptosis through loss of membrane potential and alterations in mitochondrial membrane permeability. Cytokines also directly cause adrenocorticotropic hormone (ACTH) release from the pituitary gland and cortisol release from the adrenal glands.
Glucocorticoids stimulate enzymes of amino-acid catabolism, while androgens increase amino-acid anabolism.[37],[38].
Iordanskiy et al.[45] suggested stressors should be minimized in patients who are typically of long-term nonprogressive disease status. Common symptoms of folliculitis include a rash, itching, pimples and pustules close to a hair follicle in the neck or genital area.
Virus transmission occurs through transfer of blood, vaginal fluid, semen, pre-ejaculate, or breast milk.
The plasma cells produce a specific antibody to the antigen it meets and secretes the antibody into body fluids. Inside the virus, a protein capsid surrounds the primary components of the virus that are essential for replication. 1 HIV isolates that are M-tropic are known as R5 viruses, while those that are T-tropic are referred to as X4 viruses. Env proteins have been associated with increased activation of caspase 3, increased Bax expression, and decreased Bcl-2 expression.
The primary modes of transmission are unprotected sex, breast milk, contaminated needles, and transmission at birth by an infected mother.
Memory cells circulate for about 1 year or longer in the blood, lymph, and tissues to respond to repeated exposure to the same antigen for a more sustained and stronger immune response. This component is very important in regards to the immune response to HIV and will be discussed in further detail. Two single strands of identical RNA with reverse transcriptase, integrase, and protease enzymes lie within the capsid.[1], [10] Other necessary proteins are encoded on the viral RNA. 1 HIV isolates that can bind to both CXCR4 and CCR5 are called X4R5.1 Other co-receptors are used by HIV, but CXCR4 and CCR5 are the most commonly used.
Simultaneously, the HIV envelope protein gp120 stimulates the HPA axis and causes additional glucocorticoid secretion. Alterations of membrane potential change the passage of ions through the membrane, initiating apoptosis in lymphocytes.
The intrinsic pathway is mediated by mitochondrial dysfunction, which is thought to be associated with translocation of members of the Bcl-2 protein family, including Bax. These proteins are commonly used as markers of increased or decreased apoptosis cellular signaling.
Nef can trigger apoptosis through the extrinsic pathway by Fas and Fas-L interactions (members of the tumor necrosis factor ligand family). In addition, Nef can trigger apoptosis through the intrinsic pathway by decreasing Bcl-2 expression in HIV infected cells. Binding of these death receptors to their ligands activates initiator capsase-8, leading to apoptotic cell death. Tat-induced apoptosis involves the intrinsic pathway which results in decreased Bcl-2 expression, increased Bax expression, and increased activation of caspase 8 and 10.
A decrease in SOD2 reduces the cell’s ability to neutralize reactive oxygen species (ROS) produced in the mitochondria, increasing the cell’s susceptibility to apoptosis. Furthermore, Vpr causes increased permeability of the inner mitochondrial membrane, swelling of mitochondria, and subsequent bursting of the outer mitochondrial membrane.



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