Voltage-sensitive potassium channels in Limulus ventral photoreceptors.

The steady-state slope conductance of Limulus ventral photoreceptors increases markedly when the membrane is depolarized from rest. The ionic basis of this rectification has been examined with a voltage-clamp technique. Tail currents that occur when membrane potential is repolarized after having been depolarized have been identified. The tail currents reverse direction at a voltage that becomes more positive when Ko is increased. Rectification is reduced by extracellular 4-aminopyridine and by intracellular injection of tetra-ethyl-ammonium (TEA). These results indicate that the membrane rectification around resting potential is due primarily to voltage-sensitive K+ channels. The increase in gK caused by depolarization is not mediated by a voltage-dependent rise in in Cai++, since intracellular injection of Ca++ causes a decrease rather than an increase in slope conductance. TEA can be used to examine the functional role of the K+ channels because it blocks them without substantially affecting the light-activated Na+ conductance. The effect of TEA on response-intensity curves shows that the K+ channels serve to compress the voltage range of receptor potentials.

CD4+ T cells are critical for corneal, but not skin, allograft rejection.

BACKGROUND: The relative contribution of CD4+ or CD8+ T cells in allograft rejection remains to be fully characterized. Some reports indicate that there is an absolute requirement for CD4+ T cells in allogeneic rejection, whereas others report that CD4-depleted mice are capable of rejecting certain types of allografts. METHODS: We compared the ability of CD4- knockout (KO), CD8- KO, and normal CD4+/CD8+ mice to reject allogeneic corneal or skin grafts. We also examined delayed-type hypersensitivity and CTL responses to donor alloantigens. RESULTS: Engraftment of C57BL/6 corneas to C.B6-(n5-7) CD4-KO mice resulted in significantly higher rates of acceptance (>85%) than either C.B6-(n5-7) CD8- KO (30%) or normal BALB/c mice (40%). Likewise, mean survival times for B6 skin grafts placed on C.B6-(n5-7) CD4- KO mice (29.2 +/- 3.5 days) were significantly increased over those of normal BALB/c mice (13.2 +/- 1 days), although most CD4- KO mice (70%) eventually reject their grafts. C.B6-(n5-7) CD4- KO mice that reject allogeneic grafts fail to develop a delayed-type hypersensitivity response, but they did demonstrate significantly greater cytotoxic T lymphocyte precursor (CTLp) frequencies than did CD4- KO mice that accepted such grafts or that were not grafted. CONCLUSIONS: This study indicates that mice lacking CD4+ T cells have a significantly impaired ability to reject corneal allografts, but are able, in most cases, to reject allogeneic skin grafts. Thus, in the absence of CD4+ T cells, the likely mechanism for rejection appears to involve the generation of CD8+ CTLs.

Immunologic modulation of virus-induced pathology in a murine model of acute herpetic retinal necrosis.

Unilateral inoculation of herpes simplex virus Type 1 (KOS strain) into the anterior chamber of BALB/c eyes produces an ocular disease with a distinctive differential pattern of retinal pathology. Specifically, the retina of the inoculated eye remains histologically intact, whereas the contralateral retina becomes necrotic. We demonstrate that retinal necrosis in opposite uninjected eyes directly correlates with the presence of herpes simplex viral antigens, whereas the intact retinas of virus-injected eyes are devoid of immunocytochemically detectable viral antigens. Immunosuppression or lack of a thymus results in bilateral retinal necrosis, with positive immunoperoxidase staining for viral antigens in both eyes. We have shown previously that retinal protection in both eyes can be restored to irradiated recipients by adoptive transfer of spleen cells from mice primed by AC injection of HSV. Our results with reconstituted and normal mice suggest that virus-mediated cytopathic effects underlie contralateral retinal necrosis since HSV antigens are localized to areas of retinal necrosis and their presence precedes the local inflammatory response; immunosuppression does not alter the development of contralateral retinal necrosis. They also indicate that ipsilateral retinal preservation reflects T cell-mediated inhibition of viral spread to retinas of injected eyes. Reconstitution of irradiated recipients with AC primed donor cells prevents immunohistochemically detectable virus and retinal necrosis in both eyes. In all experimental groups we failed to detect viral antigens in the absence of retinal pathology.

An immunogenetic analysis of resistance to herpes simplex virus retinitis in inbred strains of mice.

Specific inbred strains of mice have been shown to vary considerably in their resistance and susceptibility to herpes simplex virus (HSV) infection. We injected 2 X 10(5) plaque forming units (PFU) of the KOS strain of HSV-1 intracamerally into one eye of BALB/c, C57Bl/6, and F1 (BALB/c X C57Bl/6) mice. HSV-1 antigens were localized in frozen sections of enucleated eyes at 10 to 14 days post-inoculation. Injected eyes of BALB/c mice showed an anterior uveitis with HSV-1 antigens in the anterior segment and an intact retina free of HSV antigens. The retina of the contralateral uninjected eye was necrotic and contained HSV-1 antigens. In both C57Bl/6 and F1 mice, HSV antigens were limited to anterior segment structures in the injected eye, whereas, in contrast to BALB/c mice, the contralateral retina appeared histologically normal and contained no viral antigens. The C57Bl/6 and F1 strains remained relatively resistant to retinal infection even if pretreated with up to 800 Rads of irradiation. The retinas of normal or sublethally irradiated C57Bl/6 and F1, but not BALB/c strains, were also resistant to intravitreal injection of HSV. These results suggest that resistance to HSV retinitis is a dominantly inherited trait, which depends only partly upon immunologic factors and may be heavily influenced by the inherent ability of host cells from different murine strains to support a productive viral infection.

T-cell mediated responses in a murine model of orthotopic corneal transplantation.

PURPOSE: To evaluate the role that delayed-type hypersensitivity (DTH) and cytotoxic T lymphocyte responses play in a murine model of orthotopic corneal allograft transplantation. METHODS: Corneal transplantation was performed by grafting C57BL/6 donor corneas into BALB/c corneal beds. After transplantation, the mice were observed by slit lamp biomicroscopy on a weekly basis and graded for signs of graft rejection and delayed-type hypersensitivity (DTH) and cytotoxic T lymphocyte (CTL) responses to donor alloantigens assessed at selected times after grafting. RESULTS: It was determined that between 40% and 65% of BALB/c mice rejected C57BL/6 corneas by 8 weeks after engraftment. Mice with opacity scores > 2 demonstrated significantly greater DTH responses than did mice with opacity scores < 2 at 2, 3, and 4 weeks after engraftment. After 4 weeks, the DTH responses for all groups were essentially the same as for naive BALB/c mice. The DTH responses were specific for C57BL/6 alloantigens and are primarily directed against non-major histocompatibility complex (MHC) C57BL/6 alloantigens and are primarily directed against non-major histocompatibility complex C57BL/6 alloantigens, as evidenced by the ability of B10.D2 cells to elicit DTH responses whereas C.B10-H-2b cells did not. However, although BALB/c mice engrafted with C57BL/6 tail skin demonstrated significantly greater CTL activity than naive BALB/c mice, there was no significant difference in CTL activity between BALB/c mice whose C57BL/6 corneal allografts displayed opacity scores greater than (rejected) or less than (accepted) 2. CONCLUSIONS: The mechanism whereby corneal allografts in this strain combination are rejected is best associated with the ability to generate strong DTH responses and not CTL activity. This DTH response also demonstrates alloantigen specificity and appears to be primarily directed against the non-MHC component of the corneal transplant.

In vitro propagation of primary and extended life span murine corneal endothelial cells.

PURPOSE: To establish primary and extended life span cell cultures of murine corneal endothelial cells for a model system investigating corneal endothelial cell replacement and the immunologic features of corneal graft rejection. METHODS: The authors have been able to grow corneal endothelium in culture by isolating adult murine Descemet's membrane and allowing the endothelial cells to proliferate from the explants. To isolate extended life span murine corneal endothelial cells, cells were infected with an adenovirus-SV40 hybrid virus (Ad12-SV40). RESULTS: The primary cells from adult corneas proliferated to passage 3 before growth arrest-senescence was observed. However, the extended life span cells remained proliferative through passage 36 and maintained a structure similar to the primary cells. Immunohistochemical analysis demonstrate that the extended life span cells are SV40 large T antigen positive, and both the primary and extended life span murine corneal endothelial cells exhibit the common expression of several growth factor receptors and TGF-beta. CONCLUSIONS: This is the first report of the isolation and culture of mouse corneal endothelial cells. Additionally, these cells have been infected with a virus carrying the SV40 large T antigen, which yields extended life span mouse corneal endothelial cells. These cells will be of interest in establishing a murine model for corneal cell transplantation, and the authors are currently establishing protocols for the specific introduction and manipulation of these cells in both in vitro and in vivo systems. These types of analyses may provide an important animal model specific to in vivo corneal endothelial cell replacement for the treatment of endothelial-related keratopathies and can be a useful model in delineating the immunologic parameters of corneal graft rejection.

Characterization of a murine model of recurrent herpes simplex viral keratitis induced by ultraviolet B radiation.

The authors characterized a murine model of herpes simplex virus (HSV) reactivation in which recurrent herpetic keratitis was obtained in up to 80% of animals. Five weeks after ganglionic latency was established in National Institutes of Health inbred mice after corneal inoculation, HSV type 1 (HSV-1) was reactivated by irradiating the previously inoculated eye with ultraviolet (UV) light. Comparison of different UV wavelengths showed UVB to be optimal for reactivation, with peak viral recurrence being induced by a total exposure of approximately 250 mJ/cm2. Reactivated infectious virus generally began to appear in trigeminal ganglia 2 days postirradiation and was subsequently detectable in the cornea by both corneal swabbing and immunostaining for viral antigens. Two consecutive outbreaks of viral recurrence at the ocular surface were induced in selected animals by serial exposure to UVB. Advantages of this model over other models of recurrent keratitis are discussed.

Corneal Langerhans cell dynamics after herpes simplex virus reactivation.

PURPOSE: The authors investigated the progressive changes in the distribution of corneal Langerhans cells (LC) after reactivation of latent herpes simplex virus type 1 (HSV-1) in mice. METHODS: After corneal inoculation of National Institutes of Health inbred mice with HSV-1 and the establishment of latency, viral reactivation was induced by irradiating the ocular surface with 250 mJ/cm2 of ultraviolet B (UV-B) light. RESULTS: Subsequent viral replication in the cornea was followed by the migration of the LC toward the paracentral and central corneal epithelium. These areas are normally devoid of LC. The number of LC in the paracentral and central regions of the eye reached a peak at day 14 post-UV-B irradiation. After UV-B irradiation of mice latently infected with HSV-1, the development of corneal stromal opacification and neovascularization closely followed the migration of LC toward the central cornea and paralleled the influx of T-cells into the corneal stroma. This pattern was not observed in irradiated uninfected mice. CONCLUSIONS: LC migrate centrally in the corneal epithelium after viral reactivation. There is a direct correlation between the number of LC in the cornea and the degree of persistent stromal opacification.

Differential expression of the complement regulatory proteins in the human eye.

PURPOSE: The presence of complement activation products in the human eye during infection or inflammation has been well described. During complement activation the host must be protected from attack against self tissue; this is achieved by three membrane-bound complement regulatory proteins: membrane cofactor protein (MCP, CD46), decay accelerating factor (DAF, CD55), and membrane attack complex inhibiting protein (CD59). This study was undertaken to analyze the expression of these proteins in the normal human eye. METHODS: Tissues were sectioned by cryostat and both polyclonal and monoclonal antibodies to MCP, DAF, and CD59 were used. Control stains were performed with nonrelevant antibodies of the same immunoglobulin subclass and normal rabbit serum as well as by omission of the primary and secondary antibodies. RESULTS: All three proteins were found to be differentially expressed in the human eye. With anti-MCP, strong staining of the corneal epithelium and weak staining of the corneal keratocytes in stroma and photoreceptor cells was observed. Staining with anti-DAF was very strong in the corneal epithelium and the ciliary body and moderate in the corneal stroma (keratocytes) and iris. In contrast, anti-CD59 stained very strongly in the corneal epithelium, corneal stroma (keratocytes), iris, choroid, and all layers of the retina, and moderately in the ciliary body. CONCLUSIONS: Identification of MCP, DAF, and CD59 in the human eye provides evidence that a regulatory system exists to protect these cells from destruction by complement-activating events. It remains to be determined if other more specialized functions exist for these proteins, especially in the case of CD59 because of its extensive expression in the retina.

IL-1 and TNF-alpha are important factors in the pathogenesis of murine recurrent herpetic stromal keratitis.

PURPOSE: To better understand the role of interleukin (IL)-1 and tumor necrosis factor (NF)alpha in recurrent herpetic stromal keratitis (HSK), the cytokine content and the effects of anti-cytokine antibodies on mouse corneas with the disease were examined. METHODS: Competitive reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent analyses of IL-1alpha and TNF-alpha content were performed on corneas removed 3, 5, 7, 10, 14, and 21 days after latently infected NIH mice were irradiated with UV-B light to reactivate herpes simplex virus (HSV). In separate experiments, mice were injected with anti-IL-1 or anti-TNF-a antibodies 1 day before and 7 days after reactivation. RESULTS: UV-B irradiation stimulated an increase in corneal IL-la mRNA in reactivated (virus shedding) mice. This increase persisted longer and was higher than in UV-B irradiated uninfected control animals. IL-1alpha and TNF-alpha protein in corneas of reactivated mice was significantly elevated on days 3 to 10 compared with day 0 levels, and exceeded levels in control corneas on the same days. Anti-IL-1 and anti-TNF-alpha antibody administration both resulted in significantly decreased virus-induced corneal opacity between 7 and 21 days after UV-B exposure. CONCLUSIONS: IL-1alpha and TNF-alpha are upregulated in corneas in mice experiencing recurrent HSK. Abrogation of virus-induced corneal disease by anti-cytokine antibodies suggests that these cytokines play important roles in the pathogenesis of recurrent disease. Therefore, neutralization of specific proinflammatory cytokines may have potential therapeutic value.

Herpes simplex virus type 1 transcription is not detectable in quiescent human stromal keratitis by in situ hybridization.

PURPOSE: The purpose of this study was to determine whether herpes simplex virus (HSV) transcripts are present in the corneas of patients with chronic herpetic stromal keratitis. METHODS: Corneal buttons from patients with a history of stromal keratitis, but no ongoing active disease, together with positive and negative control tissues, were analyzed by in situ hybridization using single-stranded RNA probes for all three classes of viral lytic cycle transcripts as well as for the latency-associated transcripts (LATs). Tissues also were screened for presence of HSV genomic DNA using the polymerase chain reaction (PCR). RESULTS: HSV DNA was detected in 7 of 13 quiescent corneas by PCR, but no viral transcripts were detected in any of these corneas by in situ hybridization. CONCLUSIONS: At the level of detection afforded by in situ hybridization, HSV persistent in scarred human corneas after stromal keratitis appears to be transcriptionally dormant. This contrasts with the situation in neurons of latently infected sensory ganglia, in which LATs are present at high levels.

Prophylactic acyclovir effectively reduces herpes simplex virus type 1 reactivation after exposure of latently infected mice to ultraviolet B.

PURPOSE: To determine the potential efficacy and anatomic sites of action of prophylactic oral acyclovir using a murine model of ultraviolet-B-induced reactivation of herpes simplex 1 keratitis. METHODS: Latent infection with herpes simplex 1 (McKrae) was established in 80 National Institutes of Health inbred strain of mice. Forty of the mice were given acyclovir orally and the other 40 latently infected mice served as controls. Mice were exposed to 250 mJ/cm2 of ultraviolet-B radiation and killed on days 1, 2, 3, and 4 after ultraviolet-B radiation. Trigeminal ganglia and eyes from these mice were homogenized and incubated on Vero cell monolayers for recovery of reactivated virus. RESULTS: Based on the recovery of infectious virus after ultraviolet-B in treated versus control groups, acyclovir effectively reduced detectable viral reactivation at both the ocular level (P = 0.003) and the ganglionic level (P = 0.025). The numbers of viral culture-positive eye and trigeminal ganglia homogenates in the control group were 11 and 6 out of 40, respectively, compared to 1 and 0 out of 40 culture-positive eye and trigeminal ganglia homogenates in the acyclovir treated mice. Therapeutic serum levels of acyclovir were confirmed by high performance liquid chromatography. In the acyclovir-tested group, the single case of viral break-through at the ocular surface was not an acyclovir-resistant mutant. CONCLUSION: Prophylactic acyclovir effectively reduces the incidence of herpes simplex virus-1 reactivation after ultraviolet-B-induced reactivation in National Institutes of Health inbred strain of mice.

Disinfection of Goldmann tonometers against human immunodeficiency virus type 1.

Goldmann tonometer tips were inoculated with 5 X 10(5) IU of cell-free or cell-associated human immunodeficiency virus type 1 (lymphadenopathy virus type 1 isolate) or 10(4) plaque-forming units of herpes simplex virus type 1 (McKrae strain) or type 2 (Hicks strain). In an effort to mimic a "worst case" clinical scenario, each respective virus was allowed to air dry on the tonometer tip for 10 minutes. Inoculated tonometers were then (1) not treated, (2) wiped with a disposable (Kim-wipe) tissue or sterile gauze; (3) wiped with sterile gauze soaked with 3% hydrogen peroxide; or (4) wiped with a 70% isopropyl alcohol swab. The hydrogen peroxide treatment and the alcohol wipes both completely disinfected the tonometer tips for human immunodeficiency virus type 1 and herpes simplex virus types 1 and 2, whereas wiping with a sterile gauze or tissue was not effective. Wiping the Goldmann tonometer tip with an isopropyl alcohol swab and then allowing the alcohol to evaporate provides a ready and efficient means of inactivating these three enveloped viruses.

Screening of myopic photorefractive keratectomy in eye bank eyes by computerized videokeratography.

BACKGROUND: In contrast to incisional keratotomy, corneas that have undergone photorefractive keratectomy may be difficult to detect by inspection with slitlamp biomicroscopy alone. Eye bank corneas that have undergone high myopic refractive surgical correction could potentially result in substantial postoperative hyperopic correction if used as donor tissue for corneal transplantation. Surface irregularities or displacement of the treated optical zone within the graft in relation to the entrance pupil of the recipient could result in significant induced astigmatism and distortion. This study examines computerized videokeratographic screening of eye bank globes as a strategy for detecting myopic photorefractive keratectomy. METHODS: Preoperative and postoperative corneal topographic maps of freshly enucleated human and rabbit eyes that have undergone myopic photorefractive keratectomy with an excimer laser were placed in a globe-fixating device and analyzed using a vertically oriented videokeratoscope. The same system was applied in an actual eye bank setting, and potentially transplantable globes from donors without a history of corneal surgery were analyzed. RESULTS: Computerized videokeratography using a vertically mounted system reliably detected photorefractive keratectomy in 12 of 12 human eye bank corneas treated by excimer photorefractive keratectomy in a range between -1.5 to -6.0 diopters. This method also detected similar changes on lased rabbit corneas enucleated 6 weeks after excimer surgery. Data processed with the tangential mode yielded a "bull's-eye" topography pattern reflecting central corneal flattening that was more sensitive in detecting myopic corrections than the conventional axial formula-based color maps. False-positive results were not detected in 96 cadaver globes sequentially screened in the eye bank. CONCLUSIONS: Computerized videokeratography represents a feasible method to screen donor globes for myopic photorefractive keratectomy as shown by the in vitro and rabbit models. However, only whole globes and not corneoscleral sections are amenable to processing with this technique. Tangential maps provided greater sensitivity in detecting low myopic corrections than the axial formula-based color maps.

Congenital idiopathic corneal endotheliopathy.

Two unrelated boys had a history of bilateral corneal clouding at birth following uncomplicated full-term gestations and spontaneous vaginal deliveries (without forceps). Clinical examinations disclosed bilateral corneal edema, no inflammation, and normal intraocular pressures. There was no history of similarly affected family members. The patients underwent penetrating keratoplasty at ages 4 months (patient 1) and 12 years (patient 2). Light and electron microscopic studies of the corneal buttons from both patients revealed areas of degeneration of the endothelium and separation of rounded endothelial cells. The morphologic features were strikingly similar to those in two acquired forms of corneal disorders--autoimmune endotheliopathy and "acute endotheliitis." Immunocytologic and in situ hybridization studies for herpes simplex virus were not consistent with either productive or latent corneal infection. Ultrastructural changes in Descemet's membrane reflect delayed or abnormal development of the postnatal nonbanded layer in patients 1 and 2, respectively. These suggest an intrauterine insult that resulted in endothelial dysfunction. The histologic and ultrastructural features of these two congenital cases are not typical of those seen in any of the recognized causes of congenital corneal clouding. We propose that these cases represent a unique congenital corneal endotheliopathy of undetermined origin.

Herpes simplex keratitis: role of viral infection versus immune response.

The cumulative clinical and experimental data regarding the role of viral infection versus the immune response in the pathogenesis of herpes simplex stromal keratitis and central disciform endotheliitis are discussed. Ultrastructural and viral isolation studies have been performed in only a limited number of cases of human stromal keratitis and disciform endotheliitis. Virus has been isolated from the minority of corneas cultured, whereas viral particles have been demonstrated in selected cases of stromal keratitis, most of which had been treated with steroids at some point in time. The possibility of corneal latency in cases of quiescent herpetic stromal keratitis will require further systematic study. Review of the experimental and clinical findings suggests a dialectical role of the immune response in limiting viral infection, while contributing to corneal opacification and scar formation.

A theory of virus-induced demyelination in the Landry-Guillain-Barré syndrome.

The Landry-Guillain-Barré syndrome (LGBS) is a demyelinating disorder of the peripheral nervous system frequently preceded by infection with common viruses. Most prevalent among these agents are herpesviruses, particularly Epstein-Barr virus (EBV) and cytomegalovirus (CMV). The specific role played by antecedent viral infection in the pathogenesis of the LGBS remains obscure. In this regard, recent studies of Marek's disease (MD) neuropathy, an avian herpesvirus-induced experimental model for the LGBS, may provide insight. The autoimmune pattern of demyelination seen in MD neuropathy is histopathologically indistinguishable from that seen in the LGBS. In this paper, a comprehensive theory is discussed regarding the pathogenetic mechanisms that may be operative in the LGBS.

Disinfection of tonometers and contact lenses in the office setting: are current techniques adequate?

PURPOSE: To determine whether routine office techniques used to disinfect tonometer prisms and trial contact lenses are sufficient to prevent transmission of ocular infections. METHOD: We reviewed the current literature on the efficacy of certain disinfection protocols against commonly encountered viral, bacterial, and fungal pathogens as well as Acanthamoeba. RESULTS: Some commonly used disinfecting solutions and techniques may be inadequate for disinfection of viruses such as hepatitis C virus and organisms such as Acanthamoeba. When used in accordance with guidelines published by the United States Centers for Disease Control and Prevention (CDC) and the American Academy of Ophthalmology (AAO), 3% hydrogen peroxide is a very effective disinfectant against a wide variety of microorganisms. Specifically, tonometer prisms disinfected by a 5-minute soak in 3% hydrogen peroxide (or 70% isopropyl alcohol or a 1:10 dilution of sodium hypochlorite) are adequately disinfected against most ocular pathogens, with the exception of Acanthamoeba. Trial contact lenses that are disinfected with a 2-hour soak in 3% hydrogen peroxide are effectively rid of all pathogens of concern. After disinfection, rigid lenses should be stored dry, and soft lenses should be stored in a sterile, preserved solution. Repeat disinfection should be routinely performed at 1-month intervals to prevent regrowth of organisms. CONCLUSION: A safe office environment can be maintained by following current CDC recommendations for disinfection, as well as instituting some additional procedures.

Air bag-related corneal rupture after radial keratotomy.

PURPOSE: We studied a case of air bag-associated corneal rupture in a patient who had previously undergone radial keratotomy surgery. METHODS: The patient was struck in the right eye when his driver's side air bag inflated during a low-speed collision. RESULTS: Inflation of the air bag resulted in rupture of the patient's right cornea. The rupture involved all but one of his old radial keratotomy wounds. CONCLUSIONS: Patients who have undergone radial keratotomy may be at increased risk for corneal rupture caused by air bag trauma. These patients may benefit by wearing protective eyewear while driving cars equipped with air bags.

Corneal iron deposits after laser in situ keratomileusis.

PURPOSE: To report the occurrence and features of corneal iron line deposition after laser in situ keratomileusis (LASIK). METHODS: We evaluated 83 eyes undergoing LASIK. Corneal iron line deposition was analyzed with respect to preoperative spherical equivalent, attempted correction, and postoperative time interval. RESULTS: Thirty-five (42.2%) of 83 eyes displayed a distinctive brown-colored corneal iron line of variable density in a ring or patch configuration near the margin of the ablated zone in the overlying corneal flap epithelium. The appearance of this iron line correlated positively with time after surgery (>3 months) and preoperative spherical equivalent (>-4.5 diopters). CONCLUSIONS: Corneal iron line deposition in a ring or patch can be associated with previous LASIK surgery. This iron deposition within the margin of the ablated zone may offer insights into the dynamics of epithelial cell hyperplasia as well as basal cell proliferation, differentiation, and migration after LASIK.